Mechanism of regulation of KIF23 on endometrial cancer cell growth and apoptosis.

Objective: Endometrial cancer, a malignant tumor in females, is increasing globally. One of the most frequent gynecological cancers. While early-stage endometrial cancers can often be cured through uterine extirpation, those diagnosed at a later stage have a poor prognosis and face treatment challenges. Consequently, further research is required to develop primary prevention strategies for high-risk women and enhance survival rates among those with endometrial cancer. Therefore, gene therapy targeting KIF23 holds promise as a advance strategy to treating endometrial cancer. Method: We utilized immunohistochemistry, Western blotting, and PCR to observe the expression of KIF23 and its associated pathway factors in endometrial cancer tissue (Ishikawa, SNGM cells, respectively). The functional roles of KIF23 were investigated through CCK-8, colony-forming proliferation assays, Transwell migration assays, and xenotransplantation in mice. Results: Immunohistochemistry analysis revealed variation in the expression ranges of KIF23 between endometrial cancer tissue and normal endometrium tissue. KIF23 downregulated reduced BAX, caspase-3 protein expression while also increasing BCL-2 protein expression. Furthermore, knockout KIF23 hinders endometrial cancer cell proliferation and migration but promotes cell death. Mechanistically, our study provides evidence that KIF23 facilitates endometrial cancer cell proliferation via activating the ERK and AKT/PI3K pathways,while concurrently impeding programmed cell death in endometrial cancer. Conclusion: Our study provides evidence supporting that KIF23 knockdown inhibits endometrial cancer. This provides valuable evidence for future research into potential treatments for this type of cancer.