miR-126-5p suppresses HeLa and Ishikawa cell proliferation and migration via the RICTOR/AKT pathway.

OBJECTIVES: Uterine cancer is a leading gynecological malignancy with increasing incidence and mortality rates, particularly in regions such as the United States and China. Despite advancements in treatment, current therapeutic strategies are often limited by tumor heterogeneity, therapy resistance, and a lack of targeted treatment options. These challenges underscore the urgent need for novel therapeutic approaches to improve patient outcomes. This study aims to investigate the role of miR-126-5p in uterine cancer pathogenesis, focusing on its potential as a therapeutic target to address these limitations. METHOD: The study employed HeLa (cervical cancer) and Ishikawa (endometrial adenocarcinoma) cell lines to evaluate the effects of miR-126-5p on cell proliferation, migration, and apoptosis. The molecular mechanisms underlying these effects were further explored by examining the involvement of the RICTOR/AKT signaling pathway. RESULT: miR-126-5p was demonstrated to significantly inhibit cell proliferation and migration while promoting apoptosis in both HeLa and Ishikawa cell lines. These effects were mediated through the RICTOR/AKT signaling pathway, with no involvement of the RICTOR/PCK pathway. CONCLUSION: The findings reveal miR-126-5p as a critical regulator of uterine cancer progression and a promising therapeutic target. By addressing the limitations of current therapies, this study provides a foundation for the development of miRNA-based treatments, offering new hope for improving outcomes in uterine cancer patients.