DNA hypermethylation of tumor suppressor genes among oral squamous cell carcinoma patients: a prominent diagnostic biomarker

Oral Squamous Cell Carcinoma is a globally revealing form of oral malignancy. Epigenetics, which studies genetic modifications in gene expression without altering the sequence of DNA, is crucial for understanding OSCC. Key epigenetic modifications such as histone modifications, DNA methylation, and microRNA regulation play significant roles in Oral carcinoma. Aberrant methylation of DNA of tumor suppressor genes which leads to their inactivation, promoting cancer development, and specific methylation patterns are emerging as biomarkers for early OSCC detection.Current treatments like surgery, radiotherapy, and chemotherapy often fall short, prompting research into epigenetic therapies. Agents like DNMT and HDAC inhibitors demonstrate the potential for reversing aberrant epigenetic patterns, perhaps reactivating silenced TSGs, and suppressing oncogenes. Despite early promise, the development of effective combination medicines and the identification of reliable biomarkers continue to present challenges.In OSCC, resistance to therapy is also influenced by epigenetic processes. Aberrant DNA methylation and changes in histone modifications impact genes involved in medication metabolism and the survival of cells. Enhancing treatment efficacy and overcoming medication resistance may be possible by recognizing and focusing on these processes. This review explores the interplay between epigenetic changes and OSCC, their role in the disease's initiation and progression, and their impact on diagnosis and treatment. It also discusses the potential of epigenetic drugs (epi-drugs) to improve diagnostic precision and treatment outcomes.