miR‑22 inhibits proliferation and invasion in estrogen receptor α-positive endometrial endometrioid carcinomas cells Retraction in /10.3892/mmr.2021.12280

Li,Shaoru; Hu,Ruili; Wang,Chuanhong; Guo,Fang; Li,Xiaoli; Wang,Shijin

doi:10.3892/mmr.2014.2123

miR‑22 inhibits proliferation and invasion in estrogen receptor α-positive endometrial endometrioid carcinomas cells

Retraction in: /10.3892/mmr.2021.12280

Authors:
- Shaoru Li
- Ruili Hu
- Chuanhong Wang
- Fang Guo
- Xiaoli Li
- Shijin Wang
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Affiliations: Department of Gynecology and Obstetrics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China, Department of Gynecology and Obstetrics, Maternal and Child Health Hospital of Zhengzhou City, Zhengzhou, Henan 450012, P.R. China, Department of Gynecology and Obstetrics, Maternal and Child Health Hospital of Fangcheng County, Nanyang, Henan 473200, P.R. China
Published online on: April 8, 2014 https://doi.org/10.3892/mmr.2014.2123
Pages: 2393-2399

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Abstract

Endometrial endometrioid carcinomas (EECs) account for >80% of endometrial carcinomas (ECs). Continuous stimulation of the endometrium by estrogen is a risk factor for the tumorigenesis of estrogen receptor (ER) α-positive EEC. MicroRNA-22 (miR-22) has been reported to be implicated in the regulation of various types of cancer and directly targets ERα. However, an exact regulatory mechanism between miR-22 and ERα in EEC has yet to be investigated. To the best of our knowledge, the present study demonstrated for the first time that the expression of miR-22 was significantly downregulated in ERα-positive EEC tissues and cell lines, RL95-2 and Ishikawa, when compared with that in normal endometrium and ERα-negative EEC samples. This indicated that miR-22 may be important in ERα-positive EEC, possibly through an estrogen-dependent mechanism. miR-22 mimics were then transfected into RL95-2 and Ishikawa cells, respectively, and revealed that the introduction of miR-22 markedly downregulated the mRNA and protein levels of ERα. Further investigation demonstrated that miR-22 was able to effectively reverse 17β-estradiol (E2)‑induced cell proliferation, cell cycle progression and invasion of ERα-positive RL95-2 and Ishikawa cells, at least partially through inhibiting the expression of Cyclin D1 as well as the secretion of matrix metalloproteinase (MMP)-2 and MMP-9. In conclusion, the present study, to the best of our knowledge, was the first to reveal an inhibitory role of miR-22 in ERα-positive EEC tissues and cells, indicating that miR-22 may be a novel candidate for the endocrine therapy of ERα-positive EEC.

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