Dear Editor, Oral squamous cell carcinoma (OSCC) is a group of very aggressive cancers that are diverse in terms of their etiolo gy, clinical presentation, and molecular makeup. Although the processes behind the development of OSCC are poor ly understood, the majority of OSCCs are linked to alcohol and tobacco use, operating both alone and in concert. This shows that the environment plays a significant role in carcinogenesis.[1] The standard chemotherapy regimen for oral cancer consists of paclitaxel, 5-fluorouracil (5-FU), and cisplatin (CDDP) either separately or in combination. [2] High-throughput genome sequencing has revealed that over 90% of the human genome consists of non-coding RNA transcripts, which do not code for proteins but play an important role in gene regulation.[3] According to high-throughput genome sequencing, more than 90% of the human genome encodes non-coding transcripts, which do not code for proteins.[4] Non-coding RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and PIWI-interacting RNAs (piRNAs), do not code for proteins but play an import ant role in regulating gene expression at the epigenetic, transcriptional, post-transcriptional, and translational lev els (Fig. 1). In oral cancer, dysregulated ncRNA expression has been associated with tumor initiation, progression, and resistance to treatment. For example, lncRNAs and miRNAs interact, with lncRNAs functioning as competitive endog enous RNAs (ceRNAs) to modify miRNA activity and alter mRNA expression in cancer cells.[5] LncRNAs, in particular, have received a lot of attention because of their roles in tumorigenesis, prognostic outcomes, oral cancer progres sion, and associated signaling pathways. These molecules have important functions in a range of physiological and pathological processes, including cancer and the complex ity of gene regulation networks. Identifying and character izing lncRNAs linked with oral cancer provides vital insights into their potential as biomarkers for early detection and targets for developing successful therapeutics, while also addressing the challenges in using ncRNAs for improved patient outcomes.[6,7] Three tumor suppressor lncRNAs (MEG3, POU3F3, and PANDAR), two metastasis-associated lncRNAs (LINC00312 and MALAT1), and six lncRNAs (CD KN2B-AS1, H19, HOTAIR, AP5M1, linc-RoR, and FALEC) are linked to cell proliferation.[8] MicroRNAs (miRNAs) have emerged as key participants in the pathogenesis of oral cancer. MicroRNAs are tiny non-coding RNA molecules that control gene expression after transcription, influencing a variety of biological and pathological processes, including cancer formation and progression. Their involvement in oral cancer emphasizes their potential as early detection biomarkers and targets for novel techniques.
Corresponding Author: Suresh Raghavi