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. 2017 Jul 25;7:6362. doi: 10.1038/s41598-017-06472-w

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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AE2 overexpression suppressed the effects of rapamycin on cell cycle progression. OVCAR3 cells were infected with pLVX-puro (Vector) or pLVX-puro /AE2 lentivirus, and then cultured for 36 h after infection. The cells were treated with DMSO or 10 μM rapamycin (Rapa) for 12 h. (A) The cell cycle progression was analyzed. Overexpression of AE2 reversed the effects of rapamycin on G1 arrest in OVCAR3 cells. (B) Protein levels of Cyclin D1, CDK4, p16, p-p70S6K1 and p70S6K1 were determined by Western blot. *P < 0.05, **P < 0.01, ***P < 0.001 versus Vector + DMSO; ^# P < 0.05, ^## P < 0.01, ^### P < 0.001 versus AE2 + DMSO; ^$ P < 0.05, ^$$ P < 0.01, ^$$$ P < 0.001 versus Vector + Rapa.