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SNF5 is Involved in Suppression of Hepatocellular Carcinoma Progression via TGF‐Beta 1 Signaling
Author(s) -
Sun Hongmiao,
Zhong Xinping,
Wang Chunyu,
Wang Shengli,
Lin Lin,
Zou Renlong,
Wu Yi,
Sun Ning,
Sun Ge,
Wen Tao,
Chi ZhiHong,
Zhao Yue
Publication year - 2016
Publication title -
the anatomical record
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.23357
Subject(s) - gene knockdown , hepatocellular carcinoma , cancer research , sorafenib , cell growth , transforming growth factor beta , tumor progression , biomarker , signal transduction , biology , apoptosis , medicine , cancer , microbiology and biotechnology , biochemistry , genetics
ABSTRACT SNF5 (SMARCB1/INI1/BAF47), a core subunit of SWI/SNF complex, has been reported to modulate cell proliferation and apoptosis. Genetic evidence has suggested that SNF5 participates in tumor suppression. However, the detailed biological function and underlying mechanisms of SNF5 in hepatocellular carcinoma (HCC) progression remain unclear. Here, SNF5 expression reduction in HCC tissues compared with the adjacent non‐cancerous tissues has been demonstrated. Importantly, the results showed that reduced SNF5 expression has a strong correlation with worse overall survival of HCC patients. The data demonstrated that knockdown of SNF5 significantly promoted cell growth and migration in Hep3B and HCCLM3 cell lines. Interestingly, it was found that SNF5 suppressed transforming growth factor‐β1 (TGF‐β1) expression, and SNF5 mRNA expression was negatively correlated with TGF‐β1 in HCC tissues. Furthermore, depletion of SNF5 attenuated the sensitivity of HCC cells to sorafenib. Thus, the data suggested that SNF5 may participate in HCC suppression, and reduced expression of SNF5 correlates with the poor differentiation and prognosis of HCC, indicating that SNF5 might be an important prognostic biomarker and promising therapeutic target for HCC. Anat Rec, 299:869–877, 2016. © 2016 Wiley Periodicals, Inc.