miR-205 promotes tumor proliferation and invasion through targeting ESRRG in endometrial carcinoma

Su,Ning; Qiu,Haifeng; Chen,Yifei; Yang,Tingting; Yan,Qin; Wan,Xiaoping

doi:10.3892/or.2013.2400

miR-205 promotes tumor proliferation and invasion through targeting ESRRG in endometrial carcinoma

Authors:
- Ning Su
- Haifeng Qiu
- Yifei Chen
- Tingting Yang
- Qin Yan
- Xiaoping Wan
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Affiliations: 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, P.R. China, Central Laboratory, International Peace Maternity and Child Health Hospital of the China Welfare Institute Affiliated to Shanghai Jiao Tong University, Shanghai 200030, P.R. China
Published online on: April 10, 2013 https://doi.org/10.3892/or.2013.2400
Pages: 2297-2302

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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.

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