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. 2017 Mar 14;23(10):1816–1827. doi: 10.3748/wjg.v23.i10.1816

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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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Activation of autophagy contributed to oxaliplatin resistance in colorectal cancer cells. A: HT29 and HT29-oxaliplatin (OXA) cells were incubated with or without 10 μmol/L OXA for 48 h, and autophagy was determined by monodansylcadaverine (MDC)-positive stained cells using flow cytometry; B: Western blotting showed a significant increase in expression of the autophagic markers LC3-II and beclin-1 in HT29 and HT29-OXA cells with or without OXA treatment. The data represent the results of three separate experiments; C: Representative electron micrographs demonstrated autophagic vacuole formation in each group. The arrows indicate the double-membrane vacuoles digesting organelles or cytosolic contents; D: Autophagy regulated chemoresistance of OXA in HT29 and HT29-OXA cells (^eP < 0.001 indicates a significant difference vs normal control; ^aP < 0.05 indicates a significant difference vs 3-MA treatment group; ^cP < 0.05 indicates a significant difference vs rapamycin treatment group).