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- Title
FSCN-1 increases doxorubicin resistance in hepatocellular carcinoma through promotion of epithelial-mesenchymal transition.
- Authors
Zhang, Yuanbiao; Lu, Yi; Zhang, Chengwu; Huang, Dongsheng; Wu, Weiding; Zhang, Yuhua; Shen, Jian; Cai, Ying; Chen, Wei; Yao, Weifeng
- Abstract
Resistance to chemotherapy drugs remains a significant problem for the treatment of many types of cancer. Fascin-1 (FSCN-1) is an actin-bundling protein involved in the invasion and metastasis of a variety of tumors. However, its involvement in drug resistance in hepatocellular carcinoma (HCC) remains unclear. The present study aimed to investigate the function of FSCN-1 in HCC resistance to doxorubicin (DOX). FSCN-1 expression was increased in DOX-resistant HCC cell lines (SNU449 and SNU387) compared with DOX-sensitive cell lines (Huh7 and Hep3B). The resistance of HCC cells to DOX was decreased following FSCN-1 knockdown with small interfering RNA. FSCN-1 knockdown also significantly altered the expression of key markers of epithelial-mesenchymal transition (EMT). Notably, vimentin expression was reduced and epithelial-cadherin expression was increased. Furthermore, when EMT was suppressed through knockdown of Twist, an essential pathway of DOX-induced EMT, the viability of HCC cells following treatment with DOX was not affected by FSCN-1 expression. Furthermore, FSCN-1 knockdown eliminated hypoxia-induced doxorubicin resistance and EMT. The results of the present study indicated that FSCN-1 expression increased DOX resistance in HCC cells via the promotion of EMT, and this phenomenon was maintained in a hypoxic environment. FSCN-1 potentially represents a novel target to overcome resistance to DOX in HCC.
- Publication
International Journal of Oncology, 2018, Vol 52, Issue 5, p1455
- ISSN
1019-6439
- Publication type
Article
- DOI
10.3892/ijo.2018.4327