Introduction: KIFC3 is a member of the kinesin family which has shown great promise in cancer therapy recently. In this study, we sought to elucidate the role of KIFC3 in the development of GC and its possible mechanisms.
Methods: Two databases and a tissue microarray were used to explore the expression of KIFC3 and its correlation with patients' clinicopathological characteristics. Cell proliferation was examined by cell counting kit-8 assay and colony formation assay. Wound healing assay and transwell assay were performed to examine cell metastasis ability. EMT and Notch signaling related proteins were detected by western blot. Additionally, a xenograft tumor model was established to investigate the function of KIFC3 in vivo.
Results: The expression of KIFC3 was upregulated in GC, and was associated with higher T stage and poor prognosis in GC patients. The proliferation and metastasis ability of GC cells were promoted by KIFC3 overexpression while inhibited by KIFC3 knockdown in vitro and in vivo. Furthermore, KIFC3 might activate the Notch1 pathway to facilitate the progression of GC, and DAPT, an inhibitor of Notch signaling, could reverse this effect.
Conclusion: Together, our data revealed that KIFC3 could enhance the progression and metastasis of GC by activating the Notch1 pathway.
Keywords: EMT; Gastric cancer; KIFC3; Notch; Oncogene.
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