microRNA‑206 overexpression inhibits cellular proliferation and invasion of estrogen receptor α‑positive ovarian cancer cells Retraction in /10.3892/mmr.2021.12279

Li,Shaoru; Li,Yan; Wen,Zhengfang; Kong,Fanjing; Guan,Xinlei; Liu,Wenhui

doi:10.3892/mmr.2014.2021

microRNA‑206 overexpression inhibits cellular proliferation and invasion of estrogen receptor α‑positive ovarian cancer cells

Retraction in: /10.3892/mmr.2021.12279

Authors:
- Shaoru Li
- Yan Li
- Zhengfang Wen
- Fanjing Kong
- Xinlei Guan
- Wenhui Liu
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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 Endocrinology, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China, School of Public Health, Shandong University, Jinan, Shandong 250100, P.R. China
Published online on: March 6, 2014 https://doi.org/10.3892/mmr.2014.2021
Pages: 1703-1708

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Abstract

The expression levels of estrogen receptor (ER α) are closely associated with estrogen‑dependent growth, invasion and response to endocrine therapy in ERα‑positive ovarian cancer. However, the underlying regulatory mechanisms remain to be fully understood. Previous studies have demonstrated that ERα is a direct target of microRNA (miR)‑206. miR‑206 has been found to be an important tumor suppressor in several cancer types, including ovarian, gastric and laryngeal cancer. However, the specific role of miR‑206 in ovarian cancer remains unclear. The aim of the present study was to investigate the role of miR-206 in ER-a positive ovarian cancer in vitro. The present study demonstrated that miR‑206 is significantly downregulated in ERα‑positive but not ERα‑negative ovarian cancer tissues, compared with normal ovarian epithelium tissue. It was also found that the expression of miR‑206 was decreased in ERα‑positive ovarian cancer cell lines, CAOV‑3 and BG‑1, compared with normal ovarian epithelium tissues. This suggests that miR‑206 may play a role in ERα‑positive ovarian cancer cells via an estrogen‑dependent mechanism. Further analysis revealed that 17β‑E2 treatment significantly promoted cellular proliferation and invasion of estrogen‑dependent CAOV‑3 and BG‑1 cells, which could be reversed by the introduction of miR‑206 mimics. In conclusion, the present study suggests that miR‑206 has an inhibitory role in estrogen‑dependent ovarian cancer cells. Thus, miR‑206 may be a promising candidate for the endocrine therapy of ERα‑positive ovarian cancer.

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