Journal
ONCOLOGY REPORTS
Volume 45, Issue 3, Pages 1105-1117Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2021.7926
Keywords
liver cancer; interleukin-6; sorafenib; drug resistance; epithelial-mesenchymal transition
Categories
Funding
- National Science Foundation for Young Scientists of China [81101851]
Ask authors/readers for more resources
Sorafenib promotes metastasis and EMT progression in liver cancer cells by increasing IL-6 expression, and the IL-6/STAT3 signaling pathway may present a novel therapeutic strategy for liver cancer.
Interleukin-6 (IL-6) is involved in various biological responses, including tumor progression, metastasis and chemoresistance. However, the role and molecular mechanism of IL-6 in the treatment of sorafenib in liver cancer remain unclear. In the present study, through western blot analysis, Transwell assay, flow cytometric assay, ELISA analysis and immunohistochemistry it was revealed that sorafenib promoted metastasis and induced epithelial-mesenchymal transition (EMT) in liver cancer cells in vitro and in vivo, and significantly increased IL-6 expression. Endogenous or exogenous IL-6 affected metastasis and EMT progression in liver cancer cells through Janus kinase 2/signal transducer and activator of transcription 3 (STAT3) signaling. Knocked out IL-6 markedly attenuated the pro-metastasis effect of sorafenib and increased the susceptibility of liver cancer cells to it. In conclusion, the present results indicated that IL-6/STAT3 signaling may be a novel therapeutic strategy for liver cancer.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available