MiR-203 inhibits estrogen-induced viability, migration and invasion of estrogen receptor α-positive breast cancer cells
Authors: Jun Lin
Shiguang Zhu
Jie Gao
Li Wang
Journal: Experimental and therapeutic medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: breast cancer; estrogen receptor α; invasion; microRNA; migration
Affiliations: Department of Breast Surgery, Yantai Yuhuangding Hospital, Yantai, Shandong 264001, P.R. China., Department of Hematology, Yantai Yuhuangding Hospital, Yantai, Shandong 264001, P.R. China.

Abstract:  Breast cancer is common in females, and accounts for a large proportion of cancer-related cases of mortality. MicroRNAs (miRs) have been found to be involved in the progression of breast cancer via mediation of tumor suppressor genes or oncogenes. Previously, miR-203 has been reported to play a suppressive role in breast cancer. In the present study, the effects of miR-203 on the malignant phenotypes of estrogen receptor α (ERα)-positive breast cancer cells were investigated. It was found that treatment with estradiol (E2) significantly enhanced the viability, migration and invasion of ERα-positive breast cancer MCF-7 cells, accompanied by the significant downregulation of miR-203 in a dose-dependent manner. Furthermore, MCF-7 cells were transfected with miR-203 mimics, resulting in a significant increase in miR-203 levels. Upregulation of miR-203 was found to significantly inhibit E2-induced upregulation of MCF-7 cell viability, migration and invasion. Upregulation of miR-203 also led to a significant decrease in the protein expression of ERα in MCF-7 cells. Using a luciferase reporter assay, ERα was identified as a direct target of miR-203 in MCF-7 cells. Finally, it was demonstrated that miR-203 was significantly downregulated in ERα-positive breast cancer tissues compared to their matched normal adjacent tissues. The expression levels of miR-203 were inversely correlated to the ERα levels in ERα-positive breast cancer tissues. Based on these results, it is proposed that miR-203 inhibits E2-induced viability, migration and invasion of ERα-positive breast cancer cells, and that this may be via direct targeting of ERα. Therefore, the present study highlights the importance of miR-203 and ERα in breast cancer progression. 

Retracted: Yes

PubPeer comments:
 Figs 1C, 3D. ![file] For comparison, Figs 2C and 5 from [Xiao, Liu Zhao (2015)] .  Cell ... invasion were then examined by conducting a ... Transwell assay in each group . ![file] *[upper]* Figs 4 C D and 5C from [Yang et al (2016)] .  Transwell assays were conducted to examine the cell invasion capacities ofA549 cells transfected with (C) miR-133b mimics and (D) FSCN1 plasmids. Non-transfected A549 cells were used as control ....  Transwell assay were conducted to examine the cell migration and invasion in each group . *[lower]* Fig 5B from [Wang et al (2016)] .  Transwell assay to determine the invasive capacity of U2OS cells transfected with miRu2011101 mimics or cu2011FOS siRNA, or cou2011transfected with miRu2011101 mimics and cu2011FOS plasmid. Magnification, x100. Control: untransfected U2OS cells . ![file] , 
 Retracted [6 August 2021] . ------------------------- Following the publication of this paper, it was drawn to the Editorsu2019 attention by a concerned reader that the Transwell cell migration assay data shown in Figs. 1C and 3D were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to *Experimental and Therapeutic Medicine*, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. ,