PMID:
Cell Biol Int. 2019 Oct 16. Epub 2019 Oct 16. PMID: 31617643
Abstract Title:
Shikonin suppresses progression and epithelial mesenchymal transition in hepatocellular carcinoma (HCC) cells via modulating miR-106b/SMAD7/TGF-β signaling pathway.
Abstract:
Shikonin is a natural naphthoquinone component with antioxidant and anti-tumor function and has been used for hepatocellular carcinoma (HCC) treatment. According to previous study, many herbs can regulate cancer cell progression by targeting the specific miRNA (Bing Liua, 2016). However, the underlying pathological mechanism of shikonin in HCC therapy is still unclear. The detection of cell growth and death rate were performed by hemacytometry and trypan blue staining, respectively. The expression of miR-106b and SMAD7 mRNA in HCC cells was evaluated by qRT-PCR. Cell proliferation, apoptosis and migration ability were measured by CCK-8, flow cytometry and transwell assay. The expression of proteins E-cadherin, N-cadherin, vimentin, SMAD7, TGF-β1, p-SMAD3, SMAD3 and GAPDH was examined by western blot. The interaction between SMAD7 and miR-106b was assessed by luciferase reporter system. Shikonin inhibited Huh7 and HepG2 cell growth in dose-dependent manner while induced cell death in time-dependent manner. In addition, the expression ofmiR-106b was reduced after shikonin treatment. Moreover, miR-106b attenuated the suppressive effects of shikonin on HCC cell migration and EMT. SMAD7 was predicted as a target of miR-106b and the prediction was confirmed by luciferase reporter system. Additionally, we observed that SMAD7 reversed the promotive effects of miR-106b on HCC cell progression and EMT. The subsequent western blot assay revealed that shikonin could modulate SMAD7/TGF-β signaling pathway by targeting miR-106b. In conclusion, Shikonin suppresses cell progression and EMT and accelerates cell death of HCC cells via modulating miR-106b/SMAD7/TGF-β signaling pathway, suggesting shikonin could be an effective agent for HCC treatment. This article is protected by copyright. All rights reserved.
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