TMED2 promotes epithelial ovarian cancer growth
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Gong Shi-Peng1,*, Chen Chun-Lin1,*, Wu Huan2,*, Meng Fan-Liang1, Chen Yong-Ning1, Zhang Ya-Di1, Zhang Guang-Ping3 and Cai Ye-Ping4
1Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P.R. China
2Department of Obstetrics and Gynecology, The Second Affiliated Hospital, Chongqing University of Medical Sciences, Chongqing 400010, P.R. China
3Department of Gynecology, People's Hospital of Huadu District, Guangzhou 510800, P.R. China
4Department of Gynecology, Maternal and Child Health Hospital of Duanzhou District, Zhaoqing 526000, P.R. China
*These authors have contributed equally to the study and should considered as co-first authors
Gong Shi-Peng, email: email@example.com
Keywords: epithelial ovarian cancer, TMED2, IGF1R, AKT, miR-30a
Received: August 06, 2017 Accepted: September 08, 2017 Published: October 06, 2017
TMED2 is involved in morphogenesis of the mouse embryo and placenta. We found that expression of TMED2 was higher in epithelial ovarian cancer tissues than normal ovarian tissues. Silencing TMED2 decreased cell proliferation, migration, and invasion. Ectopic expression of TMED2 increased cell proliferation, migration and invasion. Silencing TMED2 inhibited ovarian cancer growth in mice. Silencing TMED2 inhibited IGF2/IGF1R/PI3K/Akt pathway. In agreement, ectopically expressed TMED2 activated IGF2/IGF1R/PI3K/Akt pathway. Mechanistic study revealed that TMED2 directly binds to AKT2, thereby facilitating its phosphorylation. We also found that TMED2 increased IGF1R expression by competing for miR-30a. Thus, TMED2 is oncogenic and a potential target for epithelial ovarian cancer therapy.
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