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BRD4 promotes tumor growth and epithelial-mesenchymal transition in hepatocellular carcinoma.
- Source :
-
International journal of immunopathology and pharmacology [Int J Immunopathol Pharmacol] 2015 Mar; Vol. 28 (1), pp. 36-44. - Publication Year :
- 2015
-
Abstract
- Bromodomain and extraterminal domain (BET) proteins are epigenetic readers that play an important role in chromatin remodeling and transcriptional regulation. In this study, we found that BRD4, a BET family member, is significantly upregulated in hepatocellular carcinoma (HCC) tissues compared with adjacent normal tissues. Furthermore, the overexpression of BRD4 in cancer tissues was correlated with poor prognosis in HCC patients. Using shRNA-mediated knockdown of BRD4 or lentivirus-mediated overexpression of BRD4 in HCC cells, we further showed that BRD4 was involved in HCC cell growth and invasion in vitro. Forced expression of BRD4 was sufficient to induce epithelial-mesenchymal transition (EMT) phenotypes in HCC cells. Additionally, BRD4 shRNA significantly inhibited HCC cell proliferation in vivo. Collectively, our study confirmed that BRD4 expression is a valuable predictor of recurrence and survival in patients with HCC. BRD4 can be further used as a potential therapeutic target of HCC.<br /> (© The Author(s) 2015.)
- Subjects :
- Cell Cycle Proteins
Cell Line, Tumor
Female
Gene Expression Regulation, Neoplastic genetics
Hep G2 Cells
Humans
Male
Middle Aged
Neoplasm Recurrence, Local genetics
Neoplasm Recurrence, Local pathology
RNA, Small Interfering genetics
Transcriptional Activation genetics
Up-Regulation genetics
Carcinoma, Hepatocellular genetics
Carcinoma, Hepatocellular pathology
Cell Proliferation genetics
Epithelial-Mesenchymal Transition genetics
Liver Neoplasms genetics
Liver Neoplasms pathology
Nuclear Proteins genetics
Transcription Factors genetics
Subjects
Details
- Language :
- English
- ISSN :
- 0394-6320
- Volume :
- 28
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- International journal of immunopathology and pharmacology
- Publication Type :
- Academic Journal
- Accession number :
- 25816404
- Full Text :
- https://doi.org/10.1177/0394632015572070