Involvement of fascin-1-mediated autophagy in the biological behavioral of endometrial cells.
10.11817/j.issn.1672-7347.2018.09.005
- Author:
Xiaomei LUO
1
;
Wei CHENG
1
;
Shizhang WANG
1
;
Zhihong CHEN
2
Author Information
1. Department of Obstetrics and Gynecology, Maternal and Child Healthcare Hospital of Hunan Province, Changsha 410008, China.
2. Department of Pathology, People's Hospital of Hunan Province, Changsha 410005, China.
- Publication Type:Journal Article
- MeSH:
Autophagy;
drug effects;
genetics;
Carrier Proteins;
genetics;
metabolism;
Cell Line;
Cell Proliferation;
drug effects;
Endometriosis;
physiopathology;
Endometrium;
cytology;
Female;
Gene Expression Regulation;
Humans;
Microfilament Proteins;
genetics;
metabolism;
Microtubule-Associated Proteins;
genetics;
RNA-Binding Proteins;
genetics;
Sirolimus;
pharmacology
- From:
Journal of Central South University(Medical Sciences)
2018;43(9):957-963
- CountryChina
- Language:Chinese
-
Abstract:
To explore the mechanism for the role of autophagy in endometriosis, and to provide a theoretical basis for prevention and treatment of endometriosis.
Methods: The endometrial CRL-7566 cells were treated with ATG5 siRNA, autophagic activator rapamycin and autophagic inhibitor 3-MA, respectively. The cell proliferation and invasion were detected by clonal formation, cell growth curve and MTT assay. The clinical specimens of endometriosis were collected from 20 cases. The expression of autophagy marker LC3II and autophagy substrate protein P62 were detected.
Results: Rapamycin inhibited the proliferation and clonal formation of CRL-7566 cells, while autophagy inhibitor 3-MA and ATG5 siRNA showed opposite effect. Moreover, rapamycin inhibited filopodia growth in endometriosis, whereas overexpression of filopodia-relevant protein fascin-1 inhibited the decrease in invasiveness caused by rapamycin. In clinical samples, we also found a significant decrease of LC3II while an increase in P62 compared with the control group.
Conclusion: Autophagy inhibition may contribute to an increase in endometrial cell proliferation and invasiveness. Autophagy activation could be a potential strategy for endometriosis therapy.
