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Upregulation of HO‐1 is accompanied by activation of p38MAPK and mTOR in human oesophageal squamous carcinoma cells
Author(s) -
Hu JianLi,
Xiao Lan,
Li ZhenYun,
Wang Qiong,
Chang Yu,
Jin Yi
Publication year - 2013
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10075
Subject(s) - pi3k/akt/mtor pathway , apoptosis , downregulation and upregulation , cell growth , squamous carcinoma , cancer research , annexin , rptor , cell cycle , biology , microbiology and biotechnology , chemistry , carcinoma , biochemistry , genetics , gene
Induction of HO‐1 protein can have both beneficial and detrimental effects for cells, including regulating proliferation and apoptosis of several tumours. We have investigated the regulation of HO‐1, p38MAPK and mTOR in the context of proliferation, cell cycle events and apoptosis of oesophageal squamous cell carcinoma cells. Real‐time PCR and Western blots were used to determine the expression levels of HO‐1, p38MAPK, p‐p38MAPK and p‐mTOR. MTT assays were used to measure proliferation, FACS for cell cycle events and Annexin V staining for apoptosis. Proliferation of Eca109 cells was inhibited and apoptosis was induced in the presence of p38MAPK inhibitor (SB203580) and mTOR inhibitor (Rapamycin, RAPA). HO‐1 expression was downregulated in cells treated with SB203580 and RAPA. HO‐1 overexpression inhibited apoptosis and induced G2/M arrest in SB203580 and RAPA‐treated cells. HO‐1 expression was upregulated in the presence of ethanol, and was accompanied by activation of p38MAPK and mTOR. However, ethanol‐treated cells exposed to HO‐1 inhibitor showed no effect on p38MAPK and mTOR activation. The data suggest that ethanol‐induced upregulation of HO‐1 in oesophageal squamous cell carcinoma is accompanied by the activation of the p38MAPK and mTOR pathways.