FGF9 promotes cisplatin resistance in colorectal cancer via regulation of Wnt/β‑catenin signaling pathway

Zhang,Zhijin; Zhang,Yuhao; Qin,Xinju; Wang,Yuexia; Fu,Jun

doi:10.3892/etm.2019.8399

FGF9 promotes cisplatin resistance in colorectal cancer via regulation of Wnt/β‑catenin signaling pathway

Authors:
- Zhijin Zhang
- Yuhao Zhang
- Xinju Qin
- Yuexia Wang
- Jun Fu
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Affiliations: Department of Gastroenterological Surgery, Shanghai Eighth People's Hospital, Shanghai 200235, P.R. China
Published online on: December 31, 2019 https://doi.org/10.3892/etm.2019.8399
Pages: 1711-1718
Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Development of cisplatin resistance in colorectal cancer is largely caused by dysregulation of signaling pathways, including the Wnt/β‑catenin signaling pathway, in cancer cells. Further investigation into the molecular mechanism of chemoresistance could improve outcomes for patients with colorectal cancer. The present study determined that fibroblast growth factor 9 (FGF9) was overexpressed in tumor tissues compared with normal tissues from patients with colorectal cancer. Using the colorectal cancer cell line LoVo, transfection of recombinant FGF9 decreased cisplatin‑induced cell apoptosis whilst FGF9 silencing increased cisplatin‑induced apoptosis. Western blot analysis and reverse transcription‑quantitative polymerase chain reaction demonstrated that FGF9 decreased adenomatous polyposis coli (APC) mRNA and protein expression and contributed to activation of the Wnt/β‑catenin signaling pathway. Notably, an increase in FGF9 and β‑catenin protein expression and a decrease in APC protein expression was observed in the established LoVo cisplatin resistant cell line (LoVo/cisplatin). Silencing of FGF9 reversed cisplatin resistance of LoVo/cisplatin cells. In conclusion, the present findings suggested that FGF9 activated the Wnt signaling pathway and was a mediator of cisplatin resistance in colorectal cancer.

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