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. 2017 Mar 15;37(5):2711–2719. doi: 10.3892/or.2017.5506

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Copyright: © Xu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — Function of GSN is regulated by miR-200a and calcium. (A) GSN expression level of 50 HCC tissues from TCGA database was higher compared with corresponding non-tumor normal tissues. P<0.05. (B) Representative images of HepG2 cell F-actin staining. Overexpression of miR-200a resulted in much more polymerized actin filaments. In the presence of Ca²⁺, the final average length of actin filaments was shorter. Treating cells with miR-200a and Ca²⁺, more polymerized actin filaments were observed. Magnification, ×400. (C) Roles of miR-200a and Ca²⁺ in regulating GSN function, in normal cells miR-200a may be the predominant regulator of GSN function and governs the secretion of MVs, while in abnormal cells the expression of miR-200a is inhibited and high level cellular Ca²⁺ activates GSN and leads to the release of more MVs.