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. 2019 Aug 19;8(13):5903–5915. doi: 10.1002/cam4.2463

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© 2019 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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The increase of HK2 dimer by GEM promoted its combining with VDAC. A, SW1990 cells were treated by GEM, mitochondrion was isolated and lysed. The interaction of HK2 dimer and VDAC was analyzed via co‐immunoprecipitation. B, MIAPaCa‐2 cells were treated by GEM, mitochondrion was isolated and lysed. The interaction of HK2 dimer and VDAC was analyzed via co‐immunoprecipitation. C, SW1990 cells were treated by GEM and GYY4137, mitochondrion was isolated and lysed. The interaction of HK2 dimer and VDAC was analyzed via co‐immunoprecipitation. D, MIAPaCa‐2 cells were treated by GEM and GYY4137, mitochondrion was isolated and lysed. The interaction of HK2 dimer and VDAC was analyzed via co‐immunoprecipitation. Abbreviations: GEM, gemcitabine; HK2, hexokinase 2; VDAC, voltage‐dependent anion channel