| Literature DB >> 18829155 |
Lin Jie Zhang1, Si Chen, Pin Wu, Chun Song Hu, Rick F Thorne, Chang Ming Luo, Peter Hersey, Xu Dong Zhang.
Abstract
We studied potential interactions between the endoplasmic reticulum (ER) stress response and the MEK/ERK pathway. Induction of ER stress did not trigger significant apoptosis, but caused rapid activation of ERK1/2 in gastric cancer cells. Inhibition of MEK enhanced ER stress-induced apoptosis via a caspase-dependent, mitochondria-mediated mechanism. This was associated with blockage of ER stress-mediated up-regulation of GRP78. The latter appeared to be critical in antagonizing the apoptosis-inducing potential of ER stress. Thus, activation of MEK/ERK by ER stress is necessary for induction of GRP78 that protects against apoptosis in gastric cancer cells submitted to ER stress.Entities:
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Year: 2008 PMID： 18829155 DOI： 10.1016/j.canlet.2008.08.030
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679