Estrogen protects SGC7901 cells from endoplasmic reticulum stress‑induced apoptosis by the Akt pathway

Fu,Zhengqi; Zou,Feng; Deng,Hao; Zhou,Hongyan; Liu,Lijiang

doi:10.3892/ol.2013.1701

Estrogen protects SGC7901 cells from endoplasmic reticulum stress‑induced apoptosis by the Akt pathway

Authors:
- Zhengqi Fu
- Feng Zou
- Hao Deng
- Hongyan Zhou
- Lijiang Liu
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Affiliations: Department of Pathology and Pathophysiology, School of Medicine, Jianghan University, Wuhan, Hubei 430056, P.R. China
Published online on: November 22, 2013 https://doi.org/10.3892/ol.2013.1701
Pages: 560-564

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Abstract

Several previous studies have demonstrated that estrogen may protect cancer cells from endoplasmic reticulum stress‑induced apoptosis. However, the molecular mechanisms involved are not fully understood. In the present study, human gastric adenocarcinoma SGC7901 cells were treated with tunicamycin (TM) to induce endoplasmic reticulum stress. This was demonstrated by increased glucose‑regulated protein 78 expression and enhanced phosphorylation of protein kinase RNA‑like endoplasmic reticulum kinase. Endoplasmic reticulum stress induced caspase‑3‑mediated apoptosis with the inhibition of Akt; the latter of which was measured by the activity‑dependent phosphorylation at Ser473 of Akt. Simultaneous treatment of 10‑9 M 17β‑estradiol (E2) with TM may protect SGC7901 cells from endoplasmic reticulum stress‑induced apoptosis by counteracting the inhibitory effect of TM on Akt, causing an increase in the phosphorylation of Ser473‑Akt. It was concluded that low concentrations of E2 may counteract endoplasmic reticulum stress‑induced inactivation of Akt to block caspase‑3‑mediated apoptosis.

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