KIF20A Promotes Malignancy and Cisplatin Resistance in Osteosarcoma by Regulating the JAK/STAT3 Signaling Pathway

Abstract

Osteosarcoma is the most prevalent primary bone cancer in both children and adolescents. One of the major clinical challenges in osteosarcoma treatment is chemoresistance, particularly resistance to cisplatin. Therefore, identifying novel biomarkers and underlying mechanisms of cisplatin resistance in osteosarcoma is imperative. In this study, we investigated the role and potential mechanisms of kinesin family member 20A (KIF20A) in cisplatin resistance in osteosarcoma. Publicly available clinical datasets were analyzed to assess the expression of KIF20A in osteosarcoma patients. Additionally, we examined the expression of KIF20A in osteosarcoma cell lines, and evaluated its functional role in cell proliferation, invasion, and cisplatin resistance in vitro. Finally, we explored the regulatory effect of KIF20A on the JAK/STAT3 signaling pathway. Our findings suggest that KIF20A is a potential regulator of osteosarcomaprogression and cisplatin resistance. Knockout of KIF20A significantly reduced the proliferation and invasion ability of osteosarcoma cells, and suppressed their resistance to cisplatin. Moreover, KIF20A was shown to regulate the oncogenic JAK/STAT3 signaling pathway. Elevated KIF20A expression enhanced osteosarcoma cell proliferation, invasion, and cisplatin resistance. This, in addition to serving as a novel biomarker for cisplatin resistance, KIF20A may represent a promising therapeutic target in osteosarcoma.