Background
Kinesin Family Member 3C (KIF3C) assumes a crucial role in various biological processes and has been engaged in the initiation and deveopment of specific human cancers. Nevertheless, there exists a paucity of systematic assessments pertaining to the contribution of KIF3C in human malignancies. Furthermore, the significance of KIF3C in the context of diagnosing and prognosticating gastric cancer (GC) has yet to be thoroughly investigated. As a result, this study endeavors to undertake a comprehensive analysis of KIF3C and assess its potential diagnostic and prognostic value in GC.
Methods
We conducted an extensive analysis of Kinesin Family Member 3C (KIF3C), covering its expression profile, prognostic relevance, molecular function, tumor immunity, and drug sensitivity. Functional enrichment analysis was also carried out for gastric cancer using publicly accessible databases. In addition, we conducted in vitro experiments to substantiate the role of KIF3C in gastric cancer (GC).
Results
KIF3C expression demonstrated consistent elevation in various tumors in comparison to their corresponding normal tissues. Our study further unveiled that heightened KIF3C expression served as a prognostic indicator, and its elevated levels correlated with unfavorable clinical outcomes, encompassing reduced OS, DSS, and PFS in several cancer types. Notably, KIF3C expression exhibited positive associations with the pathological stages of BLCA, BRCA, COAD, COADREAD, KIRP, LIHC, LUNG, and THCA. Furthermore, KIF3C expression displayed distinct associations with 60 immune checkpoints, immunoregulators, TMB, and MSI. Moreover, KIF3C demonstrated varying relationships with the infiltration of various distinct immune cell types in gastric cancer. Functional analysis outcomes indicated that KIF3C played a role in the PI3K-AKT signaling pathway. Our analysis of drug sensitivity unveiled a positive relationship between KIF3C in gastric cancer and the IC50 values of the majority of identified anti-cancer drugs. Additionally, our cellular experiments demonstrated that KIF3C knockdown reduced the proliferation, migration, and invasion capabilities, increased apoptosis, and led to alterations in the cell cycle of gastric cancer cells.
Conclusion
Our research has revealed the significant and functional role of KIF3C as an tumorigenic gene in diverse cancer types. Additionally, we observed elevated KIF3C level in gastric cancer cells, and this upregulation was notably linked to an unfavorable prognosis among gastric cancer patients. These findings indicate that KIF3C may serve as a promising target for the treatment of gastric cancer.