MiR-1202 increases radioresistance in nasopharyngeal carcinoma by targeting NAIF1/MAPK/ERK pathway

Radiotherapy is a primary treatment for nasopharyngeal carcinoma (NPC), yet intrinsic and acquired radioresistance limits therapeutic efficacy. Here, we investigated the functional role and mechanism of miR-1202 in NPC radioresponse. Using in vitro cell models and in vivo xenografts, we show that miR-1202 overexpression enhances cell survival, clonogenic capacity, and tumor growth following ionizing radiation (IR), whereas miR-1202 suppression produces the opposite effects. Mechanistically, miR-1202 directly targets NAIF1, leading to activation of the MAPK/ERK signaling pathway and modulation of apoptosis-related proteins, characterized by increased Bcl-2 and decreased BAX expression under IR. Notably, miR-1202 regulates ERK1/2 phosphorylation without affecting total ERK1/2 levels, indicating post-translational control of pathway activation. These findings identify a miR-1202-NAIF1-MAPK/ERK regulatory axis that contributes to NPC radioresistance and highlight miR-1202 as a potential biomarker and therapeutic target to improve radiotherapy outcomes.