| Autor: |
Wei, Shuxin, Lu, Chunmiao, Mo, Shutian, Huang, Hailian, Chen, Meifeng, Li, Shuai, Kong, Luping, Zhang, Hao, Hoa, Pham Thi Thai, Han, Chuangye, Luo, Xiaoling |
| Zdroj: |
Anti-Cancer Drugs; March 2024, Vol. 35 Issue: 3 p237-250, 14p |
| Abstrakt: |
In the treatment of unresectable advanced hepatocellular carcinoma (HCC), cisplatin is administered transhepatic arterially for local treatment, but the clinical application of cisplatin drugs is frequently hindered by the emergence of drug resistance. Kinesin family member 2C(KIF2C) has been shown as oncogene in a variety of tumors. Nevertheless, its effect on cisplatin sensitivity has yet to be ascertained. Herein, we aim to investigate the impact of the KIF2Cgene on cisplatin sensitivity within HCC and the plausible underlying molecular mechanism. We examined the expression level of the KIF2Cgene in HCC cells by real-time quantitative reverse transcription PCR and Western blot analysis, and analyzed bioinformatically by The Gene Expression Omnibus database and The Cancer Genome Atlas database. The KIF2Cgene was silenced using the small interfering RNA technology, and its effect on cisplatin drug sensitivity in HCC cells was evaluated by flow cytometry, cell proliferation, cell migration, and invasion assays. Our results indicated that KIF2Cwas highly expressed in HCC cells. KIF2Csilencing inhibits HCC cell proliferation, migration and invasion, promotes apoptosis, and keeps the cell cycle in G2 phase. In addition, KIF2Csilencing enhanced the sensitivity of HCC cells to cisplatin. KIF2Csilencing down-regulates the expression levels of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT) and mitogen-activated protein kinase 3 (MAPK3) proteins. In conclusion, KIF2Csilencing amplifies the sensitivity of HCC cells to cisplatin by regulating the PI3K/AKT/MAPK signaling pathway. Consequently, targeting KIF2Cshows great application potential as a strategy for enhancing the effectiveness of HCC treatment. |
| Databáze: |
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