Endometrial cancer (EC) is a common gynecological malignancy with increasing incidence, yet its precise pathogenesis remains unclear. MicroRNAs (miRNAs) have been widely implicated in tumorigenesis. Although studies suggest that miR-196b is closely associated with the progression of various malignancies, its specific biological functions and mechanisms in EC remain to be elucidated. In this study, analysis of tissue and serum samples from EC patients revealed that miR-196b is downregulated in EC, whereas GATA6 is upregulated, with a notable negative correlation between their expression levels. In Ishikawa and HEC-1 A EC cell lines, functional assays including CCK-8, colony formation, wound healing, and Transwell experiments revealed that downregulation of miR-196b significantly enhanced cell proliferation, migration, and invasion. A nude mouse xenograft model further confirmed that high miR-196b expression weakened the tumorigenic ability of EC cells. Mechanistically, dual-luciferase reporter assays identified GATA6 as a direct target of miR-196b. Downregulation of miR-196b facilitated the proliferation, metastasis, and epithelial-mesenchymal transition (EMT) of EC cells by up-regulating GATA6. The miR-196b/GATA6 axis is involved in regulating the activity of the AKT/ERK signaling pathway. Furthermore, through a series of bioinformatics analyses, we found that miR-196b and GATA6 have potential as diagnostic and prognostic markers for EC. This study elucidates the molecular mechanism by which miR-196b suppresses EC progression by targeting GATA6. These findings provide novel insights into the pathogenesis of EC and highlight the potential of miR-196b/GATA6 as a diagnostic and prognostic biomarker.
Guo et al. (2026) studied this question.