期刊
CELL CYCLE
卷 14, 期 24, 页码 3885-3896出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2015.1120917
关键词
Competing endogenous RNA; Long non-coding RNA; Liver fibrosis; Metastasis-associated lung adenocarcinoma transcript 1; MicroRNA-101b
类别
资金
- National Natural Science Foundation of China [81000176/H0317, 81100292/H0317, 81500458/H0317]
- Key Disciplines in Colleges and Universities of Zhejiang Province
- Wang Bao-En Liver Fibrosis Foundation [20120127]
- Zhejiang Provincial Natural Science Foundation of China [Y2090326, Y2110634, LY16H030012]
- Wenzhou Municipal Science and Technology Bureau [Y20110033, Y20120127]
- Incubator Program of the First Affiliated Hospital of Wenzhou Medical University [HFY2014045]
Emerging evidence shows that Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a pivotal role in cell proliferation, migration, and invasion in tumors. However, the biological role and underlying mechanism of MALAT1 in liver fibrosis remains undefined. In this study, up-regulation of MALAT1 was observed in fibrotic liver tissues and in activated hepatic stellate cells (HSCs). In addition, depletion of MALAT1 inhibited the activation of HSCs in vitro and attenuated collagen deposits in vivo. Our results demonstrated that MALAT1 expression is negatively correlated with microRNA-101b (miR-101b) expression. Furthermore, there was a negative feedback loop between the levels of MALAT1 and miR-101b. Luciferase reporter assay indicated that MALAT1 and RAS-related C3 botulinum substrate 1 (Rac1) are targets of miR-101b. We uncovered that MALAT1 regulates Rac1 expression through miR-101b as a competing endogenous RNA (ceRNA), thereby influencing the proliferation, cell cycle and activation of primary HSCs. Collectively, The ceRNA regulatory network may prompt a better understanding of liver fibrogenesis and contribute to a novel therapeutic strategy for liver fibrosis.
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