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iPadForums.net is not affiliated with Apple. We are an enthusiast site dedicated to everything Apple iPadThe advent of the Internet and the World Wide Web (the “Web”) has provided, for the first time in the history of civilization, a truly global medium of communication and information distribution. The early development of the Web was, and continues to be, driven by technology that allows for web sites to be replicated on any Web server, wherever the server may be, by providing an address to each page on a web site. For example, web sites are now published for individuals, families, small businesses, educational institutions, and governmental agencies. Due to the ubiquity of the Internet, there is very little need to build a web site for a particular location or locality. Thus, it is no longer cost-effective to build special-purpose web sites.
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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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