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. 2017 Jun 21;23(23):4243–4251. doi: 10.3748/wjg.v23.i23.4243

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©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

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miR-382 induced cell cycle arrest at G2/M phase in Eca109 cells. A and B: Cell cycle distribution of miR-382 overexpressed Eca109 cells and control cells was analyzed by flow cytometry at post-culture 48 h; C: Relative cell distribution percentage of LV-miR-382 expressed Eca109 cells to LV-Con control cells in each cell cycle phase. The data presented is mean ± SD of three independent experiments. ^aP < 0.05, vs control; D: Protein expression level of p21Cip1/Waf1 was examined in LV-Con Eca109 cells and LV-miR-382 Eca109 cells. β-actin was as a loading control.