Author/Authors :
Zhang، نويسنده , , Lin Jie and Chen، نويسنده , , Si and Wu، نويسنده , , Pin and Hu، نويسنده , , Chun Song and Thorne، نويسنده , , Rick F. and Luo، نويسنده , , Chang Ming and Hersey، نويسنده , , Peter and Zhang، نويسنده , , Xu Dong، نويسنده ,
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.
Keywords :
MEK/ERK , GRP78 , ER stress , apoptosis , Gastric cancer
