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World J Gastroenterol. Dec 14, 2013; 19(46): 8619-8629
Published online Dec 14, 2013. doi: 10.3748/wjg.v19.i46.8619
Published online Dec 14, 2013. doi: 10.3748/wjg.v19.i46.8619
P115 promotes growth of gastric cancer through interaction with macrophage migration inhibitory factor
Xiu-Jun Li, Yong-Fen Yi, Department of Pathology, Chongqing Medical University, Chongqing 400016, China
Yi Luo, Department of Obstetrics and Gynecology, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
Author contributions: Li XJ performed the majority of experiments and wrote the manuscript; Luo Y revised the manuscript; Yi YF designed the study.
Correspondence to: Dr. Yong-Fen Yi, Department of Pathology, Chongqing Medical University, No. 1, Yixueyuan Road, Chongqing 400016, China. yiyongfen@hotmail.com
Telephone: +86-23-68485868 Fax: +86-23-68485868
Received: May 30, 2013
Revised: September 24, 2013
Accepted: September 29, 2013
Published online: December 14, 2013
Processing time: 201 Days and 20.1 Hours
Revised: September 24, 2013
Accepted: September 29, 2013
Published online: December 14, 2013
Processing time: 201 Days and 20.1 Hours
Core Tip
Core tip: Gastric cancer is one of the most common cancers. P115 is a tether protein which plays a key role in cell proliferation through combination with binding partners, including migration inhibitory factor (MIF). The present study showed that P115 and MIF were specifically expressed in gastric cancer tissues and cells. P115 promoted cell proliferation and G0-G1 to S phase transition. Cell cycle regulators, including cyclin D1, Mcm2, PCNA, pERK1/2 and p53 were up-regulated by P115. P115 interacted with MIF and stimulated the secretion of MIF into the culture supernatant. In summary, P115 promotes proliferation of gastric cancer cells through an interaction with MIF.