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\title{Eminence Grise of the Genome: Long Non-Coding Ribonucleic Acids in Oral Squamous Cell Carcinomas}
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             \author[1]{Dr. Reshma  Venugopal}

             \author[2]{Dr. Radhika Manoj  Bavle}

             \author[3]{Dr. Sudhakara  Muniswamappa}

             \author[4]{Dr. Soumya  Makarla}

             \affil[1]{  Krishnadevaraya College of Dental Sciences}

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\date{\small \em Received: 12 December 2019 Accepted: 4 January 2020 Published: 15 January 2020}

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\begin{abstract}
        


Non-coding ribonucleic acids (ncRNAs) are a class of RNA molecules that are transcribed but not translated into proteins, but they affect various cellular processes. Around 60% of genes in humans do not code proteins but regulate target gene expression. Presently, a lot of research is carried out on ncRNA involvement in oral squamous cell carcinoma (OSCC) and its precursor lesions termed as oral potentially malignant disorders (OPMDs). They are broadly classified as small ncRNAs (sncRNA) and long ncRNAs (lncRNA). sncRNAs are extensively studied, whereas the divulgence of lncRNAs in OSCCs needs more revelation, hence reviewed in the present article. LncRNAs have a base pair length of more than 200, can form complex structures and influence the gene expression in a multifaceted pattern that attracts interest.

\end{abstract}


\keywords{oral squamous cell carcinoma, potentially malignant disorders, non-coding RNAs, long non-coding RNAs, competing endogenous RNA.}

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\let\tabcellsep& 	 	 		 
\section[{Introduction}]{Introduction}\par
ral Squamous cell carcinoma (OSCC) is a heterogenous malignancy which results in decreased survival rates due to local recurrence and lymph node metastases \hyperref[b0]{[1]}. Various other cancers like lymphomas and certain sarcomas possess relatable gene alterations for which effective target drug therapies are developed, but due to complex genomic and epigenomic changes and interactions in OSCC, use of an effective chemotherapeutic agent is still a challenge. Recent research has now focused on epigenomic modifications that effect the gene expression rather than gene mutations to understand these complex mechanisms \hyperref[b1]{[2,}\hyperref[b2]{3,}\hyperref[b3]{4]}. In context to this, non-coding ribonucleic acids (ncRNAs, previously considered as "junk or transcriptional noises") that are transcripts not translated to proteins but are potential effectors of target gene expression have gained additional interest \hyperref[b4]{[5,}\hyperref[b5]{6]}.\par
Statistics of Ensemble 1 show that around 34\% of the human genome are protein-coding genes. Among which 66\% of genes encode ribonucleic acids (RNAs) that are not translated into proteins \hyperref[b4]{[5,}\hyperref[b5]{6]}. The Encyclopedia of DNA Elements Consortium (ENCODE) revealed that humans have 60554 genes out of which 19815 are protein-coding genes, and the rest represents ncRNAs that regulate gene expression involved in vital physiological and pathological processes \hyperref[b3]{[4,}\hyperref[b6]{7]}.\par
They are grouped as house-keeping ncRNAs and regulatory ncRNAs. The house-keeping RNAs include ribosomal [rRNAs], transfer RNAs [tRNAs], small nuclear RNAs [snRNAs] and small nucleolar RNAs  {\ref [snoRNAs]}. The regulatory ncRNAs are divided into: a) Short ncRNAs: size < 200 base pairs (bp); b) Long nc 25 RNAs (lncRNA): size > 200 bp; c) Pseudogenes; d) Circular RNAs; e) Intronic RNAs \hyperref[b6]{[7,}\hyperref[b4]{5,}\hyperref[b5]{6]}.\par
The small ncRNAs include small interfering RNAs (siRNAs), PIWI-interacting RNAs (piRNAs), micro RNAs (mi RNAs) and transcription initiator RNAs (tiRNAs) \hyperref[b4]{[5,}\hyperref[b2]{3]}.\par
Dr. Reshma Venugopal ? , Dr. Radhika Manoj Bavle ? , Dr. Sudhakara Muniswamappa ? \& Dr. Soumya Makarla ? There are about 16,000 lncRNA genes that encode 28,000 lncRNAs. Five types of lncRNA are identified based on the position of DNA protein-coding strands [Figure \hyperref[fig_0]{1a}] from which they are synthesized.  Figure  {\ref 1d}: Intergenic lncRNA synthesized from within 1 kb of protein coding on same strand e) Intronic lncRNAs: overlapping either the sense or antisense intronic areas of the protein-coding genes (Figure  {\ref 1e}) \hyperref[b6]{[7,}\hyperref[b7]{8,}\hyperref[b8]{9]}.\par
Figure  {\ref 1e}: Intornic lncRNA synthesized from intronic region of coding gene either same or opposite side\par
LncRNAs regulate gene expression through epigenetic regulation (chromatin modification \& DNA methylation), transcription, and post transcription processing by acting as scaffolds, guides, decoys or repressors, sponges serving as competing endogenous RNAs (ceRNAs) for signaling pathways, and enhancer RNAs. They are involved in pre-mRNA splicing [Table \hyperref[tab_0]{1}] \hyperref[b0]{[1,}\hyperref[b3]{4,}\hyperref[b5]{6,}\hyperref[b8]{9,}\hyperref[b6]{7,}\hyperref[b9]{10,}\hyperref[b10]{11,}\hyperref[b11]{12,}\hyperref[b12]{13]}.  
\section[{LncRNAs scaffolds}]{LncRNAs scaffolds}\par
Platforms on which multiple enzymatic proteins can be transiently assembled in functional units such as ribonucleoprotein complex (RNP), heterogenous nuclear ribonucleoproteins (hnRNAs) etc. Their interaction is dynamic and exerts regulatory functions during mRNA processing. 
\section[{2.}]{2.}\par
LncRNAs guides Physically direct the RNAs to specific genomic region by binding to regulatory or enzymatically active proteins such as transcription factors, chromatin modifiers etc and regulate gene expression either in cis or trans sites. 
\section[{3.}]{3.}\par
LncRNA decoys Limit the availability of specific regulatory factors by acting as a molecular sink and sequester RNA-binding proteins, transcription factors, microRNAs, catalytic proteins and subunits of larger modifying complexes. They titrate these factors away from interacting with their native targets, decreasing their bioavailability, inhibiting their normal functions 4.\par
LncRNA sponges Impair miRNAs, explained by competing endogenous RNA (ceRNA) hypothesis.\par
According to which lncRNAs sequester miRNAs and reduce the availability of miRNA for the target mRNAs. The miRNAs play an important role in post transcriptional regulation of protein coding genes and mRNAs. LncRNAs actively compete with specific protein-coding mRNA that interact with intracellular pool of miRNAs acting as sponges or ceRNA for miRNAs, silence them and reduce the post-transcriptional activity. 
\section[{5.}]{5.}\par
Signalling lncRNAs Associated with specific signalling pathways or events such as cellular stress leading to transcription activation of specific genes. 
\section[{6.}]{6.}\par
Enchancer IncRNAs Enhance and promote gene activity by altering the 3 dimensional configuration of DNA.\par
LncRNAs act in nucleus or cytoplasm or both, exhibiting three types of interactions: RNA-RNA, RNA-DNA, and 52 RNA-proteins. Their partners of communication include RNA binding proteins (RBPs), transcription factors, chromatin-modifying complexes, nascent RNA transcripts, mature mRNA, microRNA, DNA, and chromatin. \hyperref[b0]{[1,}\hyperref[b6]{7,}\hyperref[b8]{9,}\hyperref[b13]{14]} In the cytoplasm, they interact with target mRNAs or miRNAs through miRNA response elements via base paring. They may stabilize or decoy the target transcripts, thus promoting or repressing the translation of transcripts to proteins \hyperref[b6]{[7]}. Cytoplasmic lncRNAs act as sponges and promote micro peptide formation \hyperref[b9]{[10,}\hyperref[b15]{16]}. 
\section[{a) Synthesis of LncRNA b) Functions of LncRNA}]{a) Synthesis of LncRNA b) Functions of LncRNA}\par
LncRNAs affect numerous biological processes such as embryological development, stem-cell biology, development, and differentiation \hyperref[b5]{[6]}. They are tissue or cell type-specific as indicated by gene expression profiling, possessing a varied expression to different pathophysiological conditions, and tumors. They regulate cell proliferation, survival, apoptosis, invasion, metastases, glycolysis, angiogenesis, growth, tumor-In the nucleus where they are mainly localized, they regulate epigenetics of protein-coding genes and alter their expression through chromatin remodeling complexes [such as polycomb repressive complex 2 (PRC 2), H3K9 methyl transferases] and DNA methylation patterns. They control the gene expression at the transcription level, act as decoys, bind to the DNA target sequences, act as alternative splicing regulators (antisense transcripts), are involved in splicing malfunctioning, and act as decoys for splicing \hyperref[b6]{[7,}\hyperref[b14]{15]}. The cis-acting lncRNAs are close to transcription site, and trans-acting lncRNAs are on distant genes of chromosomes \hyperref[b0]{[1]}.\par
LnRNAs originate and are predominantly located in the nucleus. Tissue specific RNA polymerase I, II or III transcribe lncRNAs.They are 5' capped, 3' polyadenylated, have exon/intron length, and undergo splicing of multiple exons through canonical genomic splice motifs. They resemble protein-coding mRNAs, but lack or have a small number of open reading frames. The exon length of lncRNA is the same as proteincoding mRNAs but has fewer exons that are less expressed than protein-coding mRNAs. As the span of lncRNA is more than 200 bp, they can fold into more complex three dimensional structures unlike, miRNA. The complex structure of lncRNAs determines their specific interaction with transcription factors, histone and chromatin-modifying genes affecting the expression level of a broad spectrum of genes \hyperref[b8]{[9,}\hyperref[b7]{8,}\hyperref[b9]{10,}\hyperref[b16]{17]}. stroma signaling or genomic stability, thus serving as potential diagnostic, prognostic biomarkers, and therapeutic targets \hyperref[b4]{[5,}\hyperref[b7]{8,}\hyperref[b9]{10,}\hyperref[b12]{13,}\hyperref[b17]{18,}\hyperref[b18]{19,}\hyperref[b19]{20]}.\par
LncRNAs are dysregulated in several neurological disorders and cancers, demonstrating both oncogenic and tumor-suppressive roles \hyperref[b11]{[12,}\hyperref[b20]{21]}. LncRNA Hox antisense intergenic RNA (HOTAIR), for example, functions as an oncogene in breast cancer, colorectal cancer, pancreatic cancer, etc, and increased levels are associated with reduced survival rates \hyperref[b19]{[20]}. On the other hand, maternally expressed gene 3 (MEG3) is up-regulated in breast, hepatic cancer, and plays an oncogenic role. In contrast, it is downregulated in tongue squamous cell carcinoma (TSCC) and plays a tumor-suppressor role \hyperref[b3]{[4]}. The present article reviews the expression of lncRNAs in OSCC mainly, with a note on its presentation in oral potentially malignant disorders (OPMDs).\par
Gibb et al. state that in the normal oral mucosa 325 lncRNAs are expressed. In OPMDs, around 164 lncRNAs are aberrantly expressed. Jia et al. studied 3590 differently expressed lncRNAs in TSCC, and found that 1785 were up-regulated, and 1805 were downregulated \hyperref[b2]{[3,}\hyperref[b3]{4,}\hyperref[b21]{22]}. Yu et al. detected 1572 abnormally expressed lncRNAs with 882 up-regulated, and 690 down-regulated lncRNAs \hyperref[b3]{[4]}. A study on head and neck squamous cell carcinoma (HNSCC) showed that 84 out of 3199 lncRNAs had an impact on survival rates of the patients \hyperref[b0]{[1]}.\par
Studies done by Gao et al. showed six upregulated lncRNAs such as lnc 122-PPP2R4-5, SPRR2D-1, FAM46A-1, BL2-4:1, and MBL2-4:3 (associated with high nodal status) in TSCC and two down-regulated lncRNA viz AL355149.1-1 and STXBP5-1 \hyperref[b16]{[17]}. 
\section[{II. LNCRNAs Upregulated during OSCC Progression}]{II. LNCRNAs Upregulated during OSCC Progression}\par
a) LncRNA H19 First identified long non-coding RNA, coded by gene H19 located in chromosome 11p15.5 in close association with insulin growth factor (IGF) 2 gene. LncRNA H19 is a transcription factor of the H19/IGF 2 genome blotting cluster, directly activated by c-MYC and down-regulated by p53 contributing to cell growth and proliferation \hyperref[b22]{[23]}.\par
The combination of H19 and enhancer of zest homolog 2 (EZH2) affects signal transduction of bcatenin/glycogen synthase kinase three beta (GSK 3b)/epithelial-mesenchymal transition (EMT) in TSCC, promoting lymph node metastasis and poor prognosis. MiRNA-138 and 630 down-regulate EZH2 and are suppressed by lncRNA H19. Thus H19 and Hox antisense intergenic RNA (HOTAIR) can up-regulate EZH2 decreasing the E-cadherin levels, enhancing the invasive potential of SCC cells with H19 expression being higher in metastatic tumors than nonmetastatic \hyperref[b22]{[23]}.\par
H19 acts as a ceRNA increasing the level of miRNA lethal(let)-7a targets, a chief regulator of highmobility group AT-hook 2 (HMGA 2) in the process of tumor metastasis. H19 / let-7a/HMGA2 / EMT axis plays a principal role in the regulation of invasion, metastasis, and is associated with poor prognosis in TSCC \hyperref[b3]{[4]}. H19 over-expression in endothelial cells stimulated angiogenesis. H19 regulates expression of tumor growth factor (TGF)-b, which promotes cancer cell migration through enhanced adhesion with extracellular molecules. Notch and hepatocyte growth factor regulated signaling of H19.\par
Blocking of Notch and HGF inhibited H19. The inhibition of H19 decreased cell resistance to Fulvestrant and Tamoxifen \hyperref[b9]{[10,}\hyperref[b21]{22,}\hyperref[b23]{24]}. Thus H19 plays a role in reducing the susceptibility of cells to chemotherapeutic drugs. 
\section[{b) Hox antisense intergenic RNA-HOTAIR}]{b) Hox antisense intergenic RNA-HOTAIR}\par
HOTAIR is highly conserved nuclear lncRNA, a transcript of 2.2 kb, transcribed from the (Homeobox C) HOX C locus at chromosome 12 but functions at transit close to HOX D locus on chromosome 2 that induces silencing of transcription \hyperref[b2]{[3]}.\par
The domain 5' of HOTAIR binds PCR 2, which includes EZH2, SUZ 12, and EED (both polycomb proteins) to the HOX D locus and inhibits its expression. EZH2 is a histone H3 lysine 27 methyl transferase (H3K27me 3) enzyme that catalyzes trimethylation of H3K27, a histone modification associated with long-term transcription repression \hyperref[b22]{[23]}. EZH2 is a critical epigenetic regulator for various biological processes such as cell proliferation, cell cycle, metastases, and oncogenesis \hyperref[b5]{[6,}\hyperref[b15]{16]}.\par
HOTAIR prefers to occupy a guanine-adenine (GA)-rich DNA motif on chromatin, which allows direct interaction of lncRNA transcript to specific genomic sites (has both cis and trans-regulatory mechanism) \hyperref[b19]{[20,}\hyperref[b22]{23]}. Also, the 3' domain of HOTAIR binds the histone demethylase lysine-specific histone demethylase (LSD)1. This evidence suggests that HOTAIR serves as a platform for two different histone modification complexes \hyperref[b2]{[3]}.\par
It promotes tumor cell invasion and metastasis by recruiting EZH2 and repressing E-cadherin in OSCC \hyperref[b10]{[11]}. HOTAIR is differently expressed in the saliva of patients with OSCC with metastases and without metastases \hyperref[b2]{[3]}. According to Dai et al., HOTAIR 7 is highly expressed in TSCC associated with cell proliferation, apoptosis, metastases, and invasion \hyperref[b3]{[4]}.\par
High expression of HOTAIR in laryngeal SCC is associated with tumor size greater than 0.9 cm, poor differentiation, lymph node metastasis, resistance to apoptosis, advanced clinical stages, and also drug resistance with EZH2 serving as a potential mediator \hyperref[b2]{[3,}\hyperref[b7]{8,}\hyperref[b19]{20]}.\par
HOTAIR is highly expressed in hypoxia and regulates angiogenesis through vascular endothelial growth factor A (VEGF A) directly through its promoter sequence or by modifying the levels of glucoseregulated protein-78 (GRP 78) and angiopoietin 2 (ANG-2) in nasopharyngeal carcinoma \hyperref[b9]{[10]}. 
\section[{c) Ferritin Heavy Chain 1 Pseudogene 3: FTH1P3}]{c) Ferritin Heavy Chain 1 Pseudogene 3: FTH1P3}\par
FTHIP3 is mapped to chromosome 2p23.3 with a length of 954 nucleotides, it is ferritin pseudogene with a misannotated 3' un-translated region (UTR), which is closely associated with iron-responsive elements (IREs). It affects the post-transcriptional structured cis-acting RNA regulatory elements in the 5' or 3' UTRs of mRNAs. FTH1P3 harbors miR-224-5p cognate site, sponging miRNA 224-5p and consequently modulates the expression of frizzled class receptor five, which acts as an oncogene in OSCC. miRNA 224-5p is a potential tumor suppressor that is suppressed by FTHIP3 in OSCC, contributing to oncogenesis.\par
FTH1P3 is coexpressed with plasminogen activator urokinase (PLAU) and targets OSCC associated genes, including matrix metallopeptidase (MMP) 1, 3, 9, PLAU and interleukin 8 (IL 8) which are essential regulators of tumorigenesis. Ectopic and overexpression of FTH1P3 facilitates cell proliferation, colony formation, tumor progression, metastases, and worsens survival rate in OSCC cases \hyperref[b5]{[6,}\hyperref[b10]{11,}\hyperref[b21]{22,}\hyperref[b22]{23,}\hyperref[b23]{24]}. 
\section[{d) Urothelial Cancer-associated 1-UCA1}]{d) Urothelial Cancer-associated 1-UCA1}\par
Located on chromosome 19p13.12, UCA1 regulates the expression of various genes mainly through wingless-homeobox gene (WNT)/ b-catenin signaling pathway. The lncRNA is upregulated in OSCC, promoting cellular proliferation and tumor-lymph nodemetastasis (TNM) staging. UCA1 functions as a sponge to miR-184 inhibiting it, miRNA-184, in turn, has an inhibitory effect on phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of Rapamycin (mTOR) signaling pathway. As a ceRNA, UCA 1 represses the effect of miRNA-184 promoting tumor progression, suppressing the influence of cisplatin-induced apoptosis and chemosensitivity in TSCC cells. UCA1 acts by inhibiting the cisplatinactivated PI3K/Akt signaling pathway, though, in TSCC, UCA1 promotes lymph node metastases more than cell proliferation.\par
In OSCC, it is co-expressed with numerous metabolism-related genes. UCA1 enhances the Warburg effect via mTOR activation followed by activation of signal transducer and activator of transcription 3 (STAT 3) and repression of miR-143. The Warburg effect results in increased hexokinase 2 (HK2) levels and a consequent increase in glycolysis.\par
Tonghan Zhang et al. discovered the regulation effects of UCA1/miR-124/Jagged 1 (JAG1) axis on tongue cancer which activates Notch pathway \hyperref[b3]{[4,}\hyperref[b4]{5,}\hyperref[b7]{8,}\hyperref[b11]{12,}\hyperref[b12]{13,}\hyperref[b13]{14,}\hyperref[b20]{21,}\hyperref[b24]{25,}\hyperref[b22]{23]}. 
\section[{e) Metastases associated lung adenocarcinoma transcript 1-MALAT1}]{e) Metastases associated lung adenocarcinoma transcript 1-MALAT1}\par
MALAT1 or nuclear enriched abundant transcript 2 (NEAT2), is a long intergenic non-coding RNA that maps on chromosome 11q13 \hyperref[b22]{[23]} and is 8.7 kb 203 long. It is very stable due to its triple-helical and nuclear retention element (ENE) like structure located in the nucleus and plays a role in RNA metabolism. Expression of cell cycle genes such as E2F1 transcription factors and the G1/S phase requires MALAT 1. It promotes mitosis through transcription factor B-MYB. MALAT-1 depleted cells are sensitive to p53 levels, indicating that p53 is one of the key molecules involved in the downstream effects of MALAT1.\par
MALAT 1 acts as a sponge to miRNA-125 b, which upregulates STAT 3 expression promoting OSCC development. It plays a role in EMT in OSCC cells, promoting cell migration and invasion. Its knockdown suppressed N-cadherin and vimentin but induced Ecadherin expression in vitro. In a tongue cancer cell line, MALAT1 targeted miRNA-124 and promoted cancer growth through modulation of JAG1. Studies have shown that upregulated MALAT 1 induced cervical lymph node metastasis in TSCC by increasing BCL2 associated X (BAX) expression.\par
Upregulated MALAT 1 interacts with EZH2 inducing b-catenin expression activating Wnt/b-catenin signaling pathway, upregulating MMP-7, inducing EMT, enhancing the invasion, and inhibiting apoptosis capacity of TSCC cells. Down-regulation of apoptosisrelated genes BNIP3L (pro-apoptotic BCL-2 family protein) and Neuregulin 1 (NRG1) is noted. Increased levels of MALAT 1 also incite mitogen activated protein kinase (MAPK) and PI3K/Akt. MALAT 1 functions as ceRNA for miRNA-320a, which suppresses forkhead box M1 (FOXMI). FOXM1 is involved in new vessel growth in hypoxic conditions associated with fibroblast growth factor-2 (FGF-2) expression \hyperref[b3]{[4,}\hyperref[b5]{6,}\hyperref[b13]{14,}\hyperref[b18]{19,}\hyperref[b20]{21,}\hyperref[b24]{25]}.\par
Emerges from chromosome 15q15.1 on the strand opposite to OIP5 gene and is involved mainly in the regulation of neurogenesis during development. OIP5-AS1 is an oncogene that serves as a ceRNA by sponging multiple miRNAs such as miR-340-5p, miR-217, miR-200b-3p, miR-223, miR-410, miR-378a, and miR-338-3p. miRNA 338-3p is a tumor suppressor that modulates the expression of neuropilin 1(NRP1). NRP1 is a co-receptor for VEGF and functions as an oncogene in multiple types of cancers. OIP5-AS1 functions as miR-338-3p 'sponge' to trigger NRP1 expression and thus the progression of OSCC. Overexpression of NRP1 promotes EMT by stimulating the nuclear factor-kappa B (NF-kb) pathway.\par
Knockdown of OIP5-AS1 decreased the levels of NRP1 and significantly inhibited OSCC cell proliferation, migration, invasion, retarded tumor growth, and colony formation \hyperref[b18]{[19]}.  
\section[{3.}]{3.}\par
Long intergenic nonprotein coding RNA 511-LINC00511 ceRNA for miRNA 765 increasing the expression of Laminin subunit gamma 2 (LAMC2), weakening the inhibitory effect of miRNA-765\par
High expression: Higher grades of dysplasia in leukoplakia and progression to malignancy. Increases cell proliferation and invasion in TSCC. An early biomarker. 
\section[{g) Colon cancer-associated transcript-1-CCAT1-S or cancer-associated region long non-coding RNA-5-CARLO-5}]{g) Colon cancer-associated transcript-1-CCAT1-S or cancer-associated region long non-coding RNA-5-CARLO-5}\par
CCAT1-S is a 2628 nucleotide lncRNA located on chromosome 8q24.21. CCAT1 mediates cell proliferation by inhibiting expression of cyclin-dependent kinase (CDK) inhibitor 1A (CDK N1A) mRNA, the main regulator of G0-G1 phase by increasing the expression of p16, p21, and p27 and thus cell proliferation. Silencing of CCAT1 by siRNA leads to induction of phase 1 cell cycle arrest, increased levels of E-cadherin, and decreased levels of fibronectin and vimentin required for EMT. CCAT1 interacts with transcriptional enhancer c-MYC promoter region through chromatin looping and increases its expression. CCAT1 functions as a ceRNA for miRNA-155-5p, let-7b-5p, and miRNA-490-3p by sequestration and miRNA-218-5p by epigenetic regulation.\par
27\% of oral tumor show overexpression of CCAT1 associated with increased expression of c-MYC; and down-regulation of miRNA-155-5p and let 7b-5p. Oral cancer patients with an increased level of CCAT1 are associated with tobacco use, poor prognosis, and aggressive phenotype \hyperref[b5]{[6]}. 
\section[{h) THOR-CG8846 gene product from transcript}]{h) THOR-CG8846 gene product from transcript}\par
CG8846-RA IGF 2 mRNA binding protein 1 (IGF2BP1), an oncogene belongs to a conserved family of RNAbinding proteins present mainly in the cytoplasm. They bind to mRNAs that regulate protein synthesis of k-RAS, MYC gene family, CD44, phosphatase and tensin homolog (PTEN) and IGF 2. It plays a pivotal role in cell proliferation, polarization, metabolism, morphology, differentiation, and migration. IGF2BP1 regulates the radio-/chemo-resistance of cancer cells by increasing the expression of multidrug resistance mutation 1 (MDR1).\par
THOR stabilizes the binding of IGF 2 mRNA with IGF2BP1. It regulates IGF2/mitogen activated kinase/extracellular signal-regulated kinases (IGF2/MEK/ERK) signal pathway in TSCC cells by increasing cell cycle-related proteins cyclin D 1 and E1. THOR functions as a negative prognostic marker by increasing cell proliferation; attenuates cisplatin sensitivity in nasopharyngeal carcinoma; regulates osteosarcoma stemness and mobility \hyperref[b25]{[26]}. 
\section[{i) Long Intergenic Non-Protein Coding RNA, Regulator}]{i) Long Intergenic Non-Protein Coding RNA, Regulator}\par
of Reprogramming-lncRNA-ROR Located on chromosome 18q21.31, LncRNA-ROR is 2.6 kb long non-coding RNA and consists of retrotransposons elements such as long interspersed nuclear elements (LINE), short interspersed nuclear elements (SINE) and long terminal repeater (LTR) elements. The location of lncRNA-ROR is a binding site for pluripotency transcription factors such as Sox2, Oct4, and Nanog. LncRNA-ROR acts as ceRNA for miRNA 145-5p at post-transcriptional level, modulating the expression of target genes c-MYC, Kl, SOX2, and Oct 4 impacting the differentiation of human embryonic stem cells. It also sponges miRNA-205 increasing the half-life of Zinc Finger E-Box Binding Homeobox 2 (ZEB2), thus promoting EMT. LncRNA-ROR is a suppressor of p53 during DNA damage by interacting with hnRNP I, thus directly inhibiting p53 mediated cell cycle arrest and apoptosis \hyperref[b5]{[6]}.\par
The other lncRNAs associated with OPMDs is presented in table 2 \hyperref[b3]{[4,}\hyperref[b26]{27,}\hyperref[b27]{28,}\hyperref[b28]{29]}; and OSCC progression in relation to angiogenesis in table 3 \hyperref[b3]{[4,}\hyperref[b5]{6,}\hyperref[b9]{10,}\hyperref[b17]{18,}\hyperref[b20]{21,}\hyperref[b22]{23,}\hyperref[b24]{25,}\hyperref[b28]{29]}, cell proliferation in table 4 \hyperref[b3]{[4,}\hyperref[b14]{15,}\hyperref[b18]{19,}\hyperref[b22]{23,}\hyperref[b24]{25,}\hyperref[b26]{27,}\hyperref[b29]{30,}\hyperref[b30]{31,}\hyperref[b32]{32]}, metastasis in table 5 \hyperref[b0]{[1,}\hyperref[b3]{4,}\hyperref[b5]{6,}\hyperref[b7]{8,}\hyperref[b15]{16,}\hyperref[b17]{18,}\hyperref[b21]{22,}\hyperref[b24]{25,}\hyperref[b30]{31,}\hyperref[b33]{33,}\hyperref[b35]{35]}, and chemoresistance in table 6 \hyperref[b3]{[4,}\hyperref[b12]{13,}\hyperref[b28]{29]}.    Decreased expression of lncRNA PTENP1 is observed in progressive OPMDs \hyperref[b4]{[5]}. d) Growth Arrest-Specific Transcript 5 antisense 1-GAS 5-AS1 GAS 5 induces apoptosis, is down-regulated in HNSCC, and is associated with poor prognosis. It predicts the response to radical chemotherapy and plays an essential role in the pathogenesis of oral submucous fibrosis (OSF) and its progression to malignancy \hyperref[b3]{[4,}\hyperref[b2]{3,}\hyperref[b7]{8,}\hyperref[b21]{22]}. 
\section[{e) Prostate Androgen Regulated Transcript 1-PART 1}]{e) Prostate Androgen Regulated Transcript 1-PART 1}\par
Located on chromosome 5q12, PART 1 functions as a ceRNA for miRNA-301b, which regulates Nuclear Receptor Subfamily 3 Group C Member 2 (NR3C2). Down-regulated NR3C2 promotes cell proliferation, EMT, and metastases. PART1/mir-301b/NR3C2 axis may be associated with TSCC. Androgens regulate PART 1 which is a tumor suppressor. Studies have found less expression of androgen receptor (AR) mRNA in OSCC specimens compared to healthy tissues. ARs might be involved in lessening the progression of OSCC and PART 1 is regulated by androgens, PART 1 study may also be involved in the pathogenesis of OSCC \hyperref[b32]{[32,}\hyperref[b38]{38]}.\par
f) Long Intergenic Non-Protein Coding RNA 472-LINC00472 LINC00472 acts as a sponge to miRNA-503 that regulates the expression of Gremlin 2, DAN Family BMP Antagonist (GREM2), which is an antagonist of bone morphogenetic proteins (BMP). BMP activates the Notch signaling pathway and Wnt/b-catenin signaling. Higher expression of LINC00472 is associated with a better prognosis \hyperref[b32]{[32]}.\par
IV. 
\section[{Applications}]{Applications}\par
Identification of up-regulated or down-regulated lncRNAs in the progression of OSCC is essential as their expression can be altered using appropriate RNA interference machinery such as short hairpin RNAs, miRNAs, siRNAs, oligonucleotides that are complimentary to target lncRNAs, etc. Molecule inhibitors that act by preventing the interaction of lncRNAs with the protein partners, blocking the binding or changing the secondary structure of the lncRNAs are tried. For instance, silencing of MALAT1 in TSCC, lung adenocarcinoma, cervical cancer, etc. by short hairpin RNA reduced the migration and invasive abilities of cancer cells. Blocking of MALAT1 increased the levels of miRNA 195, which decreased PDL-1 expression in B-cell lymphoma cases, decreasing apoptosis of CD 8+ cells; proliferative and metastatic abilities of the cancerous cells \hyperref[b39]{[39]}. Down-regulation of UCA1, MALAT1, HOTAIR, and FOXCUT by using siRNAs resulted in decreased cell proliferation and increased apoptosis in OSCC \hyperref[b7]{[8]}. lncRNAs are used as gene therapy drugs to deplete cancer stem cells or reverse their phenotype, thus increasing their sensitivity to radiation and chemotherapy \hyperref[b1]{[2]}.\par
V. 
\section[{Conclusion}]{Conclusion}\par
LncRNAs function as regulators in the conversion of OPMDs to OSCC, affect angiogenesis, cell proliferation, metastases, and predict chemoresistance.\par
Through reverse-transcriptase polymerase chain reaction, they can be detected in plasma and saliva, and thus serve as biomarkers. Identification of PAC3 in saliva helps in early diagnosis of OSCC, salivary gland tumors, and metastatic disease \hyperref[b7]{[8]}. Markers such as LINC00974 and NEAT 1 etc, predict the progression of OPMDs. Expression of lncRNAs such as HOTAIR, MALAT 1, etc. found in saliva can help predict metastatic status in OSCC cases. High levels of CILA 1, KCNQ1OT1, etc. predict chemoresistance in OSCC cases. Studies have found that specific siRNAs are used to alter the lncRNAs, regulating their expression in OSCC cases that works for a better prognosis. These features facilitate a thought to research these lncRNAs for good treatment options.\begin{figure}[htbp]
\noindent\textbf{1a}\includegraphics[]{image-2.png}
\caption{\label{fig_0}Figure 1a :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{1c}\includegraphics[]{image-3.png}
\caption{\label{fig_1}Figure 1c :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{1} \par 
\begin{longtable}{P{0.12934782608695652\textwidth}P{0.5728260869565217\textwidth}P{0.14782608695652172\textwidth}}
Sl no\tabcellsep Action type Long non-coding RNA\tabcellsep Function\\
1.\tabcellsep \tabcellsep \end{longtable} \par
 
\caption{\label{tab_0}Table 1 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{2} \par 
\begin{longtable}{P{0.01125\textwidth}P{0.12625\textwidth}P{0.01\textwidth}P{0.36875\textwidth}P{0.30375\textwidth}P{0.01375\textwidth}P{0.01125\textwidth}P{0.005\textwidth}}
Sl no\tabcellsep \multicolumn{2}{l}{Name of Lnc RNA}\tabcellsep Function\tabcellsep \multicolumn{3}{l}{Expression in OPMDS/OSCC}\\
1.\tabcellsep Nuclear\tabcellsep enriched\tabcellsep Oncogene regulates miR365/ Regulator of G\tabcellsep \multicolumn{4}{l}{Over expression: transformation of OPMD to}\\
\tabcellsep \multicolumn{2}{l}{abundant transcript 1-}\tabcellsep protein signalling 20 (RGS20) pathway and\tabcellsep \multicolumn{4}{l}{OSCC. Elevating proliferation, invasion,}\\
\tabcellsep NEAT 1\tabcellsep \tabcellsep up regulates cyclin dependent kinase (CDK)\tabcellsep \multicolumn{4}{l}{nodal metastases and inhibiting apoptosis in}\\
\tabcellsep \tabcellsep \tabcellsep 6 through miRNA-107\tabcellsep \multicolumn{2}{l}{OSCC. Not found in saliva.}\tabcellsep \\
2.\tabcellsep \multicolumn{2}{l}{Long intergenic non-}\tabcellsep Oncogene-Areca nut constituents have\tabcellsep Higher\tabcellsep expression:\tabcellsep increases\tabcellsep oral\\
\tabcellsep \multicolumn{2}{l}{protein coding RNA}\tabcellsep shown to activate the TGF-/p-Smad2\tabcellsep \multicolumn{4}{l}{fibrinogenesis in OSF and mediates}\\
\tabcellsep \multicolumn{2}{l}{974-LINC00974}\tabcellsep pathway mediated by LINC00974, leading to\tabcellsep \multicolumn{3}{l}{progression of OSF to OSCC.}\\
\tabcellsep \tabcellsep \tabcellsep enhanced myofibroblastic activity\tabcellsep \tabcellsep \tabcellsep \end{longtable} \par
 
\caption{\label{tab_1}Table 2 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{3} \par 
\begin{longtable}{P{0.17556980056980057\textwidth}P{0.31844729344729344\textwidth}P{0.009686609686609686\textwidth}P{0.0006054131054131054\textwidth}P{0.011502849002849003\textwidth}P{0.33418803418803417\textwidth}}
1. Hyaluronan synthase 2\tabcellsep \multicolumn{2}{l}{Marker for hypoxia}\tabcellsep \tabcellsep \tabcellsep Increased HAS2-AS1induces HIF-1a increased\\
antisense 1-Lnc HAS2-\tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep production of hyaluronan synthase which inturn\\
AS1\tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep increases EMT and OSCC tumour metastases.\\
2. HIF-1a co-activating\tabcellsep \multicolumn{4}{l}{Complexes with HIF-1a, recruitment of}\tabcellsep Complex is induced by hypoxia, stabilizing and\\
RNA-lncRNA HIFCAR\tabcellsep \multicolumn{4}{l}{HIF1a and p300 that target promoters}\tabcellsep \\
\tabcellsep in OSCC.\tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
3. Long intergenic non-\tabcellsep \multicolumn{4}{l}{Acts as a ceRNA for miRNA-297 which}\tabcellsep Up regulation: Associated with cell proliferation,\\
coding RNA 668-\tabcellsep inhibits\tabcellsep VEGF\tabcellsep A\tabcellsep promoting\tabcellsep tumor invasion of OSCC. Knockdown suppressed\\
LINCO 0668\tabcellsep \multicolumn{2}{l}{angiogenesis}\tabcellsep \tabcellsep \tabcellsep tumor growth and reduced the expression of\\
\tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep proliferation antigen ki-67\\
4. FOX C1 upstream\tabcellsep \multicolumn{4}{l}{Influences the expression of matrix}\tabcellsep Over-expressed in OSCC, associated with cell\\
transcript-FOXCUT or\tabcellsep \multicolumn{4}{l}{metalloproteins (MMP) 2, 7, 9 and}\tabcellsep proliferation, angiogenesis, colony formation and\\
long intergenic non-\tabcellsep VEGF A\tabcellsep \tabcellsep \tabcellsep \tabcellsep invasion.\\
protein coding RNA\tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
1379-LINC01379\tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
5. Long non-coding RNA\tabcellsep \multicolumn{4}{l}{Hypoxia-inducible lncRNA and acts as}\tabcellsep Enhanced levels are associated with poor clinical\\
MIR31\tabcellsep HIF-1?\tabcellsep \multicolumn{2}{l}{co-activator}\tabcellsep increasing\tabcellsep outcomes and poor prognosis in oral cancer.\\
\tabcellsep \multicolumn{2}{l}{angiogenesis}\tabcellsep \tabcellsep \tabcellsep \\
6. Long non coding RNA\tabcellsep \multicolumn{4}{l}{Binds to hnRNP-K complex and}\tabcellsep Up regulated in OSCC\\
p 21-LncRNA-p21\tabcellsep \multicolumn{4}{l}{suppresses the expression of p53}\tabcellsep \\
\tabcellsep \multicolumn{4}{l}{regulated genes. Induced by hypoxia}\tabcellsep \\
\tabcellsep \multicolumn{4}{l}{inducible factor-1a (HIF 1a) directly}\tabcellsep \\
\tabcellsep \multicolumn{4}{l}{during hypoxia, increases levels of}\tabcellsep \\
\tabcellsep \multicolumn{4}{l}{GLUT-1 and lactate dehydrogenase in}\tabcellsep \\
\tabcellsep \multicolumn{4}{l}{turn increasing glycolysis in cancer}\tabcellsep \\
\tabcellsep cells.\tabcellsep \tabcellsep \tabcellsep \tabcellsep \end{longtable} \par
 
\caption{\label{tab_2}Table 3 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{4} \par 
\begin{longtable}{P{0.19250461254612547\textwidth}P{0.3132610701107011\textwidth}P{0.31169280442804426\textwidth}P{0.032541512915129155\textwidth}}
\multicolumn{3}{l}{Eminence Grise of the Genome: Long Non-Coding Ribonucleic Acids in Oral Squamous Cell Carcinomas}\tabcellsep \\
\tabcellsep \multicolumn{2}{l}{activating HIF1-a resulting in angiogenesis}\tabcellsep \\
\tabcellsep \tabcellsep \tabcellsep 2020\\
\tabcellsep \tabcellsep \tabcellsep Year\\
\tabcellsep \tabcellsep \tabcellsep 41\\
1. Colon Cancer Associated Transcript\tabcellsep Regulates WNT/b-catenin/ GSK-3b\tabcellsep Increased expression: Cell proliferation, higher grade of tumour cell and pathological\tabcellsep Volume XX Issue V Version I\\
2-CCAT2\tabcellsep \tabcellsep affect metastases. stage (stage II/III) of OSCC, but does not\tabcellsep D D D J D )\\
2. Long intergenic non-\tabcellsep Targets miR-328-5p and miR-939-5p\tabcellsep Up regulation enhances cell proliferation\tabcellsep (\\
protein coding RNA 939 or lncRNA RP5-916L7.2 3. Cancer Susceptibility 9-CA SC 9 4. MYC-induced long non-coding RNA-MINCR 5. Long non-coding RNA Protein Disulfide Isomerase Family A Member 3 Pseudogene 1-LncRNA PDIA3P\tabcellsep Regulation of p-AKT, p-mTOR, P62 and BCL-2 Oncogene: activates the Wnt/?-catenin signalling pathway Up regulates miR-185-5p target gene cyclin D2 (CCND2) by competitively sponging miR-185-5p and then activating CCND2 signalling pathways involved in cell cycle progression from G1 to S phase\tabcellsep and inhibits cell apoptosis in TSCC. Over expression: Inhibition of apoptosis, promotes cell proliferation, increases local recurrence in OSCC cases. High expression: promotes cell proliferation Up-regulation results in OSCC cell proliferation, tumor growth, increased Ki-67 index and decreased the survival rates. Prognostic biomarker to distinguish patients with higher risks of OSCC progression. and regulates G0/G1 stage in OSCC.\tabcellsep Global Journal of Medical Research\\
6. Long non-coding RNA\tabcellsep Induced by higher levels of notch 1. Acts a\tabcellsep Upregulated TUG increased cell proliferation\tabcellsep \\
Taurine upregulated\tabcellsep sponge of miR-145 that regulates Wnt/b-\tabcellsep and decreased apoptosis.\tabcellsep \\
gene 1-LncRNA TUG 1\tabcellsep catenin signalling pathway. TUG 338\tabcellsep \tabcellsep \\
\& 338\tabcellsep dysregulated down stream factors STAT 1,\tabcellsep \tabcellsep \\
\tabcellsep ATK and caspase 3.\tabcellsep \tabcellsep \\
7 Long Intergenic non-\tabcellsep Regulates expression of Ectonucleotide\tabcellsep Up-regulation inhibits apoptosis. Decreased\tabcellsep \\
coding RNA 261-\tabcellsep Pyrophosphatase/ Phosphodiesterase\tabcellsep expression shows better prognosis in TSCC\tabcellsep \\
LINC00261\tabcellsep (ENPP) 4 and ENPP5 that are involved in\tabcellsep \tabcellsep \\
\tabcellsep tumor development. Low expression of\tabcellsep \tabcellsep \\
\tabcellsep ENPP2 increases reactive oxygen species\tabcellsep \tabcellsep \\
\tabcellsep level that promotes tumor cell apoptosis.\tabcellsep \tabcellsep \\
\tabcellsep \tabcellsep © 2020 Global Journals\tabcellsep \end{longtable} \par
 
\caption{\label{tab_3}Table 4 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{5} \par 
\begin{longtable}{P{0.017694846407717693\textwidth}P{0.061931962427011926\textwidth}P{0.11372175679106372\textwidth}P{0.36339172378776335\textwidth}P{0.29325971058644323\textwidth}}
\tabcellsep 1\tabcellsep HOXA transcript at the\tabcellsep Activation of HOX A gene\tabcellsep High expression: advanced clinical stage,\\
\tabcellsep \tabcellsep distal tip-HOTTIP\tabcellsep \tabcellsep tumour size and metastases. Independent\\
\tabcellsep \tabcellsep \tabcellsep \tabcellsep prognostic factor\\
\tabcellsep 2\tabcellsep A disintegrin and\tabcellsep ce RNA for miRNA 600 which\tabcellsep Up regulation decreased miR-600 levels,\\
\tabcellsep \tabcellsep metalloproteinase with\tabcellsep reduces EZH2 levels\tabcellsep increasing EZH2 function, promoting migration\\
\tabcellsep \tabcellsep a thrombospondin type\tabcellsep \tabcellsep and invasion through TGF-b1 mediated EMT\\
\tabcellsep \tabcellsep 1 motif 9 antisense 2-\tabcellsep \tabcellsep process in TSCC. Expression being more in\\
\tabcellsep \tabcellsep ADAMTS9-AS2\tabcellsep \tabcellsep lymph node metastatic TSCC than non-\\
\tabcellsep \tabcellsep \tabcellsep \tabcellsep metastatic TSCC.\\
\tabcellsep 3\tabcellsep Krueppel-like factor 8\tabcellsep KLF8 binds to the upstream\tabcellsep Upregulation: promoted cell migration and EMT\\
\tabcellsep \tabcellsep (KLF 8) regulated Long\tabcellsep sequence of AC132217.4, activating\tabcellsep by upregulating IGF2, activating AKT signalling\\
\tabcellsep \tabcellsep non coding\tabcellsep its expression and interacts with the\tabcellsep in OSCC promoting lymph node metastases.\\
Year 2020\tabcellsep 4.\tabcellsep AC132217.4 Long Intergenic Non-Protein Coding RNA\tabcellsep 3' UTR of IGF2 mRNA increasing its stability, leading to increased IGF2 ceRNA for miRNA 185-5p, silencing YWHAZ, that promotes apoptosis levels\tabcellsep Up regulation of LINC00958 downregulates YWHAZ promoting proliferation and metastases\\
\tabcellsep \tabcellsep 958-LINC00958\tabcellsep and inhibits cell proliferation.\tabcellsep of OSCC.\\
Volume XX Issue V Version I\tabcellsep 5. 6. 7. 8.\tabcellsep Long intergenic non-protein-coding RNA 673-LINC00673 Long intergenic non-coding RNA 00152-LINC00152 Small nucleolar RNA host gene 20-LncRNA SNHG20 Long non coding RNA small nucleolar RNA host gene 1-lncRNA\tabcellsep \multicolumn{2}{l}{Action in OSCC yet to be determined. Up regulation: increases tumour size, muscle infiltration, clinical stage, survival and recurrence rate in TSCC. Early biomarker for OSCC. Binds to EZH2, silences the expression of p15 and p21 inducing tumor cell cycle progression High expression: correlates with TSCC progression, advanced stage, relapse and invasion. Regulates SNHG20/miR-197/LIN 28 axis Over expression: higher TNM stage, lesser tumor differentiation and poor overall survival in OSCC. Sponge for miR-195-5p leading to over expression of Notch2 and Hes Up regulation: enhances cell growth, invasion and EMT in esophageal squamous cell cancer.}\\
( D D D D ) J\tabcellsep 9.\tabcellsep SNHG 12 Long non coding\tabcellsep Promotes mechanical expression of\tabcellsep High levels associated with cell proliferation,\\
Medical Research\tabcellsep \multicolumn{2}{l}{HNF1A antisense RNA 1-LncHNF1A-AS1 10. Colorectal Neoplasia Differentially Expressed-CRNDE 11. Cancer Susceptibility}\tabcellsep Notch 1 and Hes 1 decreases expression of miRNA 384 which targets Kristen rat sarcoma (K-RAS), cell division cycle (CDC) 42 and insulin receptor substrate 1 (IRS 1) genes inhibits miRNA-33a-5p\tabcellsep migration and poor prognosis in OSCC. Up-regulation: Accelerates the cell cycle, promotes the proliferation and invasion in TSCC. Increased levels promotes proliferation and\\
Global Journal of\tabcellsep \multicolumn{2}{l}{15-CA SC 15 12. Lnc GIF2IRD2P1 and lnc PDIA3F 13. Lnc RNA GIHCG 14. X-inactive specific transcript-XIST}\tabcellsep Targets MMP 3, 9, PLAU, IL-8 and PDIA3P GIHCG is the gene inhibitor of miR-200b/200a/429 expression and inhibits expression of miRNA 429 regulates oncogene E2F3 by spongeing miR-34a-5p and miR-137\tabcellsep migration in TSCC cells Over expression: progression and metasatses of OSCC. Up-regulation: accelerates cell cycle, promotes proliferation and metastasis in TSCC. Up-regulation: promotes cell growth, EMT and poor overall survival of HNSCC.\\
\tabcellsep \multicolumn{2}{l}{15. Deleted in lymphocytic}\tabcellsep Increases the expression of\tabcellsep Over expression: increases proliferation,\\
\tabcellsep \tabcellsep leukemia 1 (DLEU 1)\tabcellsep hyaluronan synthase 3 (HAS 3) and\tabcellsep migration, invasion, metastasis, xenograft\\
\tabcellsep \tabcellsep \tabcellsep CD 44 and interacts with HA-CD44\tabcellsep formation, inhibits apoptosis and leads to\\
\tabcellsep \tabcellsep \tabcellsep signalling. upregulates CDH1 that\tabcellsep progression in OSCC cells.\\
\tabcellsep \tabcellsep \tabcellsep codes for E-cadherin.\tabcellsep \\
\tabcellsep \multicolumn{2}{l}{16. Long intragenic non-}\tabcellsep NAG7 transcript is translated into\tabcellsep Up-regulation: inhibits proliferation (G1/S arrest)\\
\tabcellsep \tabcellsep coding RNA 312-\tabcellsep protein-estrogen receptor\tabcellsep and increases cell adhesion, motility and\\
\tabcellsep \tabcellsep LINC00312 or NAG7\tabcellsep repressor-10 (ERR-10) and functions\tabcellsep invasion. Positively correlates with lymphnode\\
\tabcellsep \tabcellsep \tabcellsep as both coding and non-coding RNA\tabcellsep metastases and negatively correlates with\\
\tabcellsep \tabcellsep \tabcellsep \tabcellsep clinical stage and tumour size.\end{longtable} \par
 
\caption{\label{tab_4}Table 5 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{6} \par 
\begin{longtable}{P{0.34122302158273377\textwidth}P{0.15838129496402878\textwidth}P{0.24276978417266187\textwidth}P{0.10762589928057553\textwidth}}
1. Chemotherapy-induced\tabcellsep \multicolumn{2}{l}{Activates Wnt/b catenin pathway}\tabcellsep High levels of CILA-1 and low levels of\\
lncRNA 1-CILA1\tabcellsep \tabcellsep \tabcellsep phosphorylated b-catenin increased cisplatin\\
\tabcellsep \tabcellsep \tabcellsep resistance in TSCC patients, promoted EMT and\\
\tabcellsep \tabcellsep \tabcellsep invasiveness.\\
2. KCNQ1 overlapping\tabcellsep \multicolumn{2}{l}{Transcriptionally silences KCNQ1}\tabcellsep High expression: chemoresistance in TSCC\\
transcript 1-KCNQ1OT1\tabcellsep locus by regulating histone\tabcellsep \\
\tabcellsep \multicolumn{2}{l}{methylation, ceRNA to miRNA 211-5p}\\
\tabcellsep \multicolumn{2}{l}{that regulates Ezrin (also known as}\\
\tabcellsep \multicolumn{2}{l}{cytovillin or villin-2) /focal adhesion}\\
\tabcellsep \multicolumn{2}{l}{kinase (Fak)/Src (non receptor tyrosine}\\
\tabcellsep kinase) signalling pathway\tabcellsep \\
3. Long non coding RNA-\tabcellsep \multicolumn{2}{l}{Possess complementary sequence to}\tabcellsep Over expression: Increased tumor size, clinical\\
lnc-p23154\tabcellsep \multicolumn{2}{l}{miR-378a-3p promoter region. miRNA}\tabcellsep stage, lymph node metastasis and decreased\\
\tabcellsep 378-3p targets 3?UTR of Glut1,\tabcellsep \tabcellsep sensitivity of phenformin in OSCC patients.\\
\tabcellsep \multicolumn{2}{l}{inhibiting its expression \& in turn}\\
\tabcellsep \multicolumn{2}{l}{glycolysis. Lnc-p23154 interacts with}\\
\tabcellsep \multicolumn{2}{l}{miR-378a-3p promoter to repress its}\\
\tabcellsep \multicolumn{2}{l}{transcription, and then increases Glut1}\\
\tabcellsep expression.\tabcellsep \\
\multicolumn{2}{l}{III. LNCRNAs Down-Regulated during}\tabcellsep \multicolumn{2}{l}{b) Nuclear 270 factor-kappa beta interacting long non-}\\
\multicolumn{2}{l}{OSCC Progression}\tabcellsep \multicolumn{2}{l}{coding 271 RNA-NKILA NKILA helps in phosphorylation of nuclear}\\
\multicolumn{2}{l}{a) Maternally expressed gene 3-MEG3}\tabcellsep \multicolumn{2}{l}{factor of kappa light polypeptide gene enhancer in B}\\
\multicolumn{2}{l}{Mapped to chromosome 14q32.2, MEG 3 is expressed in normal human tissues and posses tumor suppressor properties. Its expression is lost, especially in cases of HPV-related OSCC due to gene deletion and promoter hypomethylation or hypermethylation of intergenic differentially methylated region. Decreased expression of MEG 3 results in the upregulation of the WNT pathway increasing the levels of b catenin. MEG3 increases the levels of p53 protein and regulates the}\tabcellsep \multicolumn{2}{l}{cells inhibitor ? (Ik??) and inhibits activation of NF-k?. Low levels in cancer promote EMT through TNF-? signaling and increase malignant potential in OPMDs. Reduced levels of NKILA are associated with decreased disease-free survival rates and overall survival rates [2,4,6]. c) Long non-coding ribo-nucleic acid phosphatase and tensin homolog pseudogene 1-lnc RNA PTENP 1:}\\
\multicolumn{2}{l}{downstream expression of p53 target genes. Notch 1}\tabcellsep \tabcellsep LncRNA PTENP1 modulates PTEN expression\\
\multicolumn{2}{l}{and Hes 1 are inhibited by MEG 3 blocking cell}\tabcellsep \multicolumn{2}{l}{by acting as a sponge for miRNA-17, miRNA-21,}\\
proliferation and metastasis.\tabcellsep \tabcellsep \multicolumn{2}{l}{miRNA-214, miRNA-19, and miRNA-26, which suppress}\\
\multicolumn{2}{l}{Studies have revealed that miRNA-26a can increase the expression of MEG3 in TSCC tissues by targeting DNA methyltransferase 3B (DNMT3B) transcript inhibiting cell proliferation and triggering}\tabcellsep \multicolumn{2}{l}{PTEN expression. Enhanced expression of PTEN can reverse the Warburg effect by PI3K independent or dependent mechanisms inhibiting glycolysis in cancer cells.}\\
\multicolumn{2}{l}{apoptosis. Down-regulation of MEG3 and miRNA-26a}\tabcellsep \\
\multicolumn{2}{l}{results in the increased malignant potential of OPMDs}\tabcellsep \\
\multicolumn{2}{l}{and poor OSCC prognosis [1,4,5,6,23].}\tabcellsep \end{longtable} \par
 
\caption{\label{tab_5}Table 6 :}\end{figure}
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\end{bibitemlist}
 			 		 	 
\end{document}
