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. 2018 Mar 1;17(5):6526–6532. doi: 10.3892/mmr.2018.8663

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Copyright: © Long 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. — miR-367 promotes PTEN expression and inhibits the phosphorylation of AKT in A375 cells, and enhanced cell proliferation. (A) Upregulation of miR-367 distinctly reduced PTEN level, promoted the phosphorylation of AKT, and increased cell proliferation. (B) Downregulation of miR-367 markedly raised the PTEN level, attenuated the phosphorylation of AKT and inhibited cell proliferation. (C) The PTEN level was significantly raised in A375 cells transfected with PTEN vectors in comparison with empty vectors group. *P<0.01, compared with miR-control group; ^#P<0.01, compared with negative control group; ^$P<0.01, compared with empty vectors group. miR, microRNA; PTEN, phosphatase and tensin homolog; AKT, protein kinase B.