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You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response or make a trackback to this entry\], and the reduced expression of miR-200c also accelerated NSCLC progression \[[@CR6]\]. We confirmed the negative correlation between miR-200c and vimentin in clinical samples. The expression of miR-200c was lower in HCCLM3-LM1 cells than in Huh7-LM3 cells, suggesting that miR-200c downregulation may contribute to EMT, invasion and chemoresistance in HCC. In the previous study of ovarian carcinoma cells, miR-200c expression was increased following treatment with a glycosylation inhibitor to restore E-cadherin expression \[[@CR30]\]. In the present study, miR-200c expression and the expression of E-cadherin were decreased in HCCLM3-LM1 cells, implying that the role of miR-200c in HCC is not limited to E-cadherin, and that regulation of miR-200c expression may be a novel way to control EMT. This may explain why miR-200c overexpression inhibits invasion and induces apoptosis in HCCLM3-LM1 cells and LM3 cells.

In our study, the expression of miR-200c in the LM3 sub-cell lines was higher than in the LM1 sub-cell lines, suggesting that the effect of miR-200c is dependent on its expression. However, the expression of other miRNAs in LM3 sub-cell lines did not differ from the LM1 sub-cell lines (Additional file [1](#MOESM1){ref-type=”media”}: Figure S1), indicating that the effect of miR-200c on hepatocellular carcinoma cells is independent of the other miRNAs. miR-200c has been shown to inhibit migration, invasion, proliferation, and chemoresistance in cancer cells \[[@CR6], [@CR31]–[@CR33]\]. In addition, in our studies, miR-200c overexpression reduced the proliferation and colony-forming ability of HCC

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