AMF/PGI-mediated tumorigenesis through MAPK-ERK signaling in endometrial carcinoma

Yiran Li; Yuanhui Jia; Qi Che; Qian Zhou; Kai Wang; Xiao-Ping Wan

doi:10.18632/oncotarget.4708

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This article has been corrected. Correction in: Oncotarget. 2020; 11:755-757.

AMF/PGI-mediated tumorigenesis through MAPK-ERK signaling in endometrial carcinoma

Yiran Li, Yuanhui Jia, Qi Che, Qian Zhou, Kai Wang _ and Xiao-Ping Wan

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Oncotarget. 2015; 6:26373-26387. https://doi.org/10.18632/oncotarget.4708

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Abstract

Yiran Li1, Yuanhui Jia2, Qi Che2, Qian Zhou2, Kai Wang2, Xiao-Ping Wan3

1Department of Obstetrics and Gynecology, Shanghai First People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai, China

2Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, China

3Department of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, China

Correspondence to:

Kai Wang, e-mail: [email protected]

Xiao-Ping Wan, e-mail: [email protected]

Keywords: endometrial carcinoma, Autocrine Motility Factor (AMF)/PhosphoGlucose Isomerase (PGI), MAPK signaling pathway, invasion, prognosis

Received: April 29, 2015 Accepted: July 08, 2015 Published: July 20, 2015

ABSTRACT

Autocrine motility factor (AMF), which is also known as phosphoglucose isomerase (PGI), enhances tumor cell growth and motility. In this study, we found that AMF and its receptor were both highly expressed in Endometrial Carcinoma (EC) tissues compared to normal tissues. Levels of AMF were increased in serum of endometrial cancer patients. Downregulation of AMF by shRNA inhibited invasion, migration and proliferation as well as growth in a three-dimensional culture. AMF cytokine function, but not enzymatic activity of PGI, regulated tumorigenic activities of AMF. The MAPK-ERK1/2 pathway contributed to AMF-induced effects in EC cells. In agreement, Mek inhibitor decreased AMF-induced invasion, migration and proliferation of EC cells. In addition, in two mouse tumor metastasis models (EC cells delivered through left ventricle or intraperitoneally) AMF-silenced EC cells showed decreased tumor proliferative and metastatic capacities. We suggest that AMF/PGI is a potential therapeutic target in endometrial carcinoma.

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AMF/PGI-mediated tumorigenesis through MAPK-ERK signaling in endometrial carcinoma

Abstract