Autophagy-mediated HMGB1 release promotes survival of gastric cancer cells via the activation of ERK1/2 MAPK kinases

ZHANG Qiuyu; WU Linqing; HAN Yangfei; XU weiqun; ZHANG Tao

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Autophagy-mediated HMGB1 release promotes survival of gastric cancer cells via the activation of ERK1/2 MAPK kinases

ZHANG Qiuyu 1 * #,WU Linqing 2,HAN Yangfei 2,XU weiqun 2,ZHANG Tao 2

1.Department of Immunology, Fujian Medical University, Fuzhou 350108；Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Fujian Medical University, Fuzhou 350108

2.Department of Immunology, Fujian Medical University, Fuzhou 350108

*Correspondence author

#Submitted by

Subject:

Funding: National Natural Science Foundation of China （No.No. 81101558), Fujian Provincial Committee of Natural Science and Technology）

Opened online:31 December 2014

Accepted by: none

Citation: ZHANG Qiuyu,WU Linqing,HAN Yangfei.Autophagy-mediated HMGB1 release promotes survival of gastric cancer cells via the activation of ERK1/2 MAPK kinases[OL]. [31 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4624561

OBJECT: To investigate the effect of extracellular high-mobility group box 1（HMGB1）on cell proliferation and signaling pathway in human gastric cancer cell. Methods: Immunohistochemistry and immunocytochemistry localized HMGB1 in gastric cancer tissues and gastric carcinoma cell lines. The protein level of microtubule light chain 3（LC3-I, LC3-II）and the formation of autophagic vesicles in gefitinib -induced BGC-823 cells were assessed by western blotting and confocal microscopy respectively. Western blot and ELISA were used to assess the effects of gefitinib, an epidermal growth factor receptor inhibitor, on autophagy and HMGB1 release in BGC-823 cells. MTT and Western blot assessed the effects of extracellular HMGB1 on cell proliferation and signaling transduction. Results: Released HMGB1 promoted proliferation through activation of ERK1/2 MAPK. HMGB1 expression in gastric cancer tissue and serum was significantly increased compared to control and healthy serum. Gastric carcinoma cells showed elevated HMGB1 in nuclei and cytoplasm, whereas GES-1 cells exhibited lower HMGB1 with nuclear localization. Gefitinib increased autophagy and cytoplasmic HMGB1 release from BGC-823 cells. Extracellular HMGB1 in autophagic cell supernatant promoted proliferation that was abolished by glycyrrhizic acid, an HMGB1 inhibitor. BGC-823 cells incubated with HMGB1 increased ERK1/2 phosphorylation, but did not affect JNK, p38 or AKT. Blocking RAGE-HMGB1 interaction with antibody or siRNA suppressed ERK1/2 activation and gastric cancer cell growth, indicating RAGE-mediated ERK1/2 signaling was necessary for tumor progression. Conclusions: Extracellular HMGB1 promoted growth through RAGE-dependent activation of ERK1/2 in gastric cancer.

Keywords:oncology; gastric cancer; HMGB1; autophagy; RAGE; ERK

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