Bai JA, Xu GF, Yan LJ, Zeng WW, Ji QQ, Wu JD, Tang QY. SGK1 inhibits cellular apoptosis and promotes proliferation via the MEK/ERK/p53 pathway in colitis. World J Gastroenterol 2015; 21(20): 6180-6193 [PMID: 26034353 DOI: 10.3748/wjg.v21.i20.6180]
Corresponding Author of This Article
Qi-Yun Tang, MD, PhD, Department of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Rd, Nanjing 210029, China. tqy831@163.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
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Bai JA, Xu GF, Yan LJ, Zeng WW, Ji QQ, Wu JD, Tang QY. SGK1 inhibits cellular apoptosis and promotes proliferation via the MEK/ERK/p53 pathway in colitis. World J Gastroenterol 2015; 21(20): 6180-6193 [PMID: 26034353 DOI: 10.3748/wjg.v21.i20.6180]
Jian-An Bai, Gui-Fang Xu, Li-Jun Yan, Wei-Wen Zeng, Qian-Qian Ji, Jin-Dao Wu, Qi-Yun Tang, Department of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China
Author contributions: Bai JA and Xu GF contributed equally to this study; Bai JA, Xu GF and Tang QY designed the research; Bai JA and Xu GF performed the research; Yan LJ, Ji QQ, Zeng WW and Wu JD contributed to the model establishment or analytic tools; Bai JA analyzed the data; Bai JA, Xu GF and Tang QY wrote the paper.
Supported by National Natural Science Foundation of China, No. 81470806; the National Natural Science Foundation of Jiangsu Province, No. BK20141496; and the Public Health Ministry of Jiangsu Province in the Talents in Medical Science Program, No. RC201179.
Ethics approval: The study was reviewed and approved by the First Affiliated Hospital of Nanjing Medical University Institutional Review Board.
Institutional animal care and use committee: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of Nanjing Medical University.
Conflict-of-interest: No conflicts of interest.
Correspondence to: Qi-Yun Tang, MD, PhD, Department of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Rd, Nanjing 210029, China. tqy831@163.com
Telephone: +86-25-68136542 Fax: +86-25-83674636
Received: October 12, 2014 Peer-review started: October 13, 2014 First decision: November 14, 2014 Revised: December 12, 2014 Accepted: February 12, 2015 Article in press: February 13, 2015 Published online: May 28, 2015 Processing time: 230 Days and 2.7 Hours
Core Tip
Core tip: This study showed that serum-and-glucocorticoid-inducible-kinase-1 (SGK1) expression was significantly increased in the inflamed epithelia of patients with active Crohn’s disease (CD) in a TNBS-induced colitis model. At the cellular level, silencing of SGK1 inhibited the phosphorylation of mitogen-activated protein kinase kinase 1 (MEK1) and the downstream molecule ERK1/2, which induced the upregulation of p53 and Bcl-2-associated X protein, triggering subsequent cellular apoptosis and inhibition of proliferation in intestinal epithelial cells. A MEK1 inhibitor (i.e., U0126) was used to show that this was a MEK/ERK-dependent process. Co-immunoprecipitation analysis uncovered the mechanism of the interaction between SGK1 and MEK1. Our results provide a new therapeutic approach to CD therapy.
