KIFC1 promotes the proliferation of hepatocellular carcinoma in vitro and in vivo
- Xing Wang
- Meng Wang
- Xing‑Yue Li
- Jian Li
- Dian‑Peng Zhao
Affiliations: Department of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261031, P.R. China
- Published online on: October 14, 2019 https://doi.org/10.3892/ol.2019.10985
Copyright: © Wang
et al. This is an open access article distributed under the
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Hepatocellular carcinoma (HCC) is a common type of malignant tumor worldwide with a high mortality rate. In the past 20 years, the morbidity rate of HCC has increased. Progress has been made in the clinical diagnosis and therapy for HCC. However, due to the high heterogeneity and metastasis targeted therapy for HCC exhibits great promise, and novel therapeutic targets for HCC are urgently required. Kinesin family member C1 (KIFC1) is a member of the kinesin superfamily of proteins. Previous studies have indicated a potential association between KIFC1 and cancer progression. However, the potential role of KIFC1 in the development of HCC remains unclear. The present study aimed to explore the function of KIFC1 in HCC. Immunohistochemical (IHC) assays were performed to explore the KIF15 expression levels in 74 samples of HCC and corresponding non‑tumor tissues. The potential association between KIF15 expression levels and clinical features was analyzed, and the effects of KIF15 on cell proliferation of HCC were detected by colony formation and MTT assays. In addition, the proliferation‑related proteins Ki67 and PCNA were detected by western blotting. The possible effects of KIF15 on tumor growth were measured in mice. The results demonstrated that a high expression level of KIFC1 was associated with poor prognosis of HCC. Further results indicated that KIFC1 promoted cell proliferation of HCC in vitro. In addition, knockdown of KIFC1 suppressed tumor formation and growth in mice. Therefore, these results provide a potential therapeutic target for the treatment of HCC.