title: miR-205 promotes tumor proliferation and invasion through targeting ESRRG in endometrial carcinoma.
abstract: Increasing evidence suggests that miR‑205 is frequently dysregulated in many types of human cancers, suggesting its important roles in the initiation and progression of cancer. However, the functions of miR‑205 in human endometrial endometrioid carcinoma (EEC) are still unknown. In this study, we investigated the expression of miR‑205 in both normal endometrium and EEC tissues using TaqMan PCR. Compared to normal tissues, miR‑205 was significantly upregulated in EEC (P<0.001). After transfection of miR‑205 inhibitors into Ishikawa cells (or transfection of miR‑205 mimics into AN3CA cells), we demonstrated that the cellular proliferation, migration and invasion properties were negatively regulated by miR‑205. Moreover, by combination of microRNA target prediction algorithms and luciferase reporter system, we identified estrogen-related receptor‑γ (ESRRG) as a target of miR‑205. In conclusion, we demonstrated frequent upregulation of miR‑205 in EEC. In gain‑of‑function and loss‑of‑function assays, inhibition of miR‑205 reduced cellular proliferation, migration and invasion; vice versa, increased levels of miR‑205 led to upregulated cellular proliferation, migration and invasion. Nonetheless, we identified the ESRRG gene to be a novel target, which could be helpful to elucidate mechanisms underlying the tumorigenesis of EEC.
authors.affiliation: Department of Obstetrics and Gynecology, International Peace Maternity and Child Health Hospital of the China Welfare Institute Affiliated to Shanghai Jiao Tong University, Shanghai 200030, PR China.
authors.forename: Ning
authors.initials: N
authors.lastname: Su
authors.forename: Haifeng
authors.initials: H
authors.lastname: Qiu
authors.forename: Yifei
authors.initials: Y
authors.lastname: Chen
authors.forename: Tingting
authors.initials: T
authors.lastname: Yang
authors.forename: Qin
authors.initials: Q
authors.lastname: Yan
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Wan
mesh_terms: D020413:3' Untranslated Regions; D001483:Base Sequence; D001665:Binding Sites; D018269:Carcinoma, Endometrioid / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D016889:Endometrial Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D005260:Female; D015870:Gene Expression; D015972:Gene Expression Regulation, Neoplastic; D057809:HEK293 Cells; D006801:Humans; D035683:MicroRNAs / Q000502:physiology*; D008969:Molecular Sequence Data; D009361:Neoplasm Invasiveness; D034622:RNA Interference; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011960:Receptors, Estrogen / Q000235:genetics* / Q000378:metabolism
chemical_list: D020413:3' Untranslated Regions; D035683:MicroRNAs; D012333:RNA, Messenger; D011960:Receptors, Estrogen; C490917:ESRRG protein, human; C534425:MIR205, human