Research Projects


 Epigenetic modifications are key regulators of immune cell function, particularly within the tumor microenvironment. Among these, RNA epigenetics refers to chemical modifications on RNA molecules that occur without altering their nucleotide sequence, yet significantly influence RNA stability, processing, localization, and translation. These modifications play crucial roles in gene expression regulation, cellular differentiation, tissue development, and the pathogenesis of various diseases. To date, numerous RNA modifications have been identified, including N6-methyladenosine (m6A), 5-methylcytosine (m5C), 1-methyladenosine (m1A), 7-methylguanosine (m7G), N4-acetylcytosine (ac4C), pseudouridine (Ψ), uridylation, and adenosine-to-inosine (A-to-I) editing. These modifications are dynamically controlled by a set of enzymes: “writers” (which catalyze the addition of modifications), “erasers” (which remove them), and “readers” (which recognize and interpret them), thereby forming a complex and finely tuned regulatory network that determines RNA fate and function. Among these, m1A modification has emerged as a significant regulator of RNA metabolism. It contributes to RNA stability, promotes protein synthesis, and modulates gene expression. m1A is predominantly enriched in the 5′ untranslated regions (UTRs) of mRNAs—especially at the first and second nucleotide positions and near the translation initiation site—where it enhances translational efficiency. It is also found within coding regions and is positively associated with protein synthesis. Beyond mRNA, m1A is commonly present in conserved positions of tRNAs, as well as in rRNA and long non-coding RNA (lncRNA). The addition of m1A to RNA is catalyzed by “writer” enzymes such as TRMT6, TRMT61A, TRMT10C, TRMT61B, BMT2, MTR1, and NML. Its removal is mediated by “erasers,” including ALKBH1, ALKBH3, ALKBH7, and FTO. The functional consequences of m1A are further executed through its recognition by “reader” proteins such as YTHDF1, YTHDF2, YTHDF3, and YTHDC1, which modulate RNA stability, translation, and degradation. In T-cells, m1A RNA methylation is increasingly recognized as a modulator of immune responses. However, its specific role in regulating T-cell proliferation and functionality in the context of cancers remains largely unexplored. Given that tumor progression often involves mechanisms of immune evasion—including the suppression of T-cell activity—understanding the epigenetic regulation of T-cells may reveal novel pathways involved in tumor immune escape. This study aims to investigate the m1A RNA methylation landscape in T-cells derived from breast/ovarian cancer patients. By elucidating the relationship between m1A modifications and T-cell function, the study seeks to uncover novel epigenetic mechanisms underlying immune dysregulation within the tumor microenvironment and to identify potential epigenetic targets for enhancing anti-tumor immunity.