KCNJ15 inhibits epithelial‑mesenchymal transition in colorectal cancer cell lines involving the PI3K/AKT/mTOR signaling pathway

KCNJ15 encodes the inwardly rectifying potassium channel Kir4.2, which is essential for maintaining cellular homeostasis and is implicated in tumor initiation and progression. In this study, we explored the expression profile, biological functions and molecular mechanisms of KCNJ15 in colorectal cancer (CRC) cells. Immunohistochemical analysis revealed that KCNJ15 was downregulated in CRC tissues, and its low expression was correlated with poor patient prognosis. We performed a series of experiments, including RT-qPCR, Western blotting, CCK-8 proliferation assay, colony formation assay, wound healing assay, and Transwell invasion assay, to verify that KCNJ15 overexpression markedly suppressed the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of CRC cells. Mechanistically, the process whereby KCNJ15 suppresses EMT involves the PI3K/AKT/mTOR signaling pathway. Taken together, our cell‑based findings indicate that KCNJ15 represents a potential therapeutic candidate for colorectal cancer.