Autocrine Motility Factor Modulates Proliferation Signaling Mediated By GPER

ABSTRACT: Traditional surgery plus radiotherapy or chemotherapy, existing targeted therapies failed to significantly improve the survival rate of recurrent endometrial cancer, so suggesting that mechanism of recurrence and progression that modulates in endometrial cancer is clinically important. Here, we show that GPER(G protein-coupled estrogen receptor 1) was binded to AMF, and the complex were translocation form plasma to cytoplasmic. Mechanistic investigations elucidated that interaction of AMF with GPER triggers phosphoinositide-3-kinase (PI3K) signaling activating and accelerating the ability of endometrial cancer cells growth. Furthermore, we found that AMF may contribute to GPER-mediated endometrial cancer progression using animal experiments and human histological experiments which be consistent with the above conclusions. On the basis of these evidences including invivo and invitro, our findings suggest that AMF–GPER interaction might be novel key molecular targets for therapeutic management of patients with endometrial cancer, whose disease were progression and recurrence.

OTHER RELATED OMICS DATASETS IN: GSE114362

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Endometrial Cancer

SUBMITTER: Yiran Li  

LAB HEAD: xiaoping wan

PROVIDER: PXD009780 | Pride | 2019-03-12

REPOSITORIES: Pride