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. 2019 May 29;18(1):435–442. doi: 10.3892/etm.2019.7629

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Copyright: © Li 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 7. — LncRNA-HOTAIR affects the PI3K/AKT/mTOR signaling pathway in DOXR-MCF-7 cells. (A) The protein expression and phosphorylation of (B) mTOR (C) PI3K and (D) AKT was assessed via western blotting. Values are expressed as the mean ± standard deviation of three independent experiments. *P<0.05 and **P<0.01 vs. the NC group. ^#P<0.05 vs. the control group. LncRNA, long non-coding RNA; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B; mTOR, mechanistic target of rapamycin; HOTAIR, HOX transcript antisense RNA; PI3K, siRNA, small interfering RNA; NC, negative control; siR, small interfering RNA.