miR-148a Suppresses estrogen-induced viability and migration of breast cancer cells via inhibition of estrogen receptor α expression
Authors: Weihui Li
Zexuan Li
Yeqian Feng
Fang Ma
Tiebang Liu
Lingjiang Li
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: breast cancer; estrogen; estrogen receptor α; microRNA-148a.
Affiliations: Mental Health Institute, The Second Xiangya Hospital, National Technology Institute of Psychiatry, Key Laboratory of Psychiatry and Mental Health of Hunan, Central South University, Changsha, Hunan 410011, P.R. China., Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China., Department of Psychiatry, Shenzhen Kangning Hospital, Shenzhen, Guangdong 518020, P.R. China.

Abstract:  MicroRNAs (miRs) play critical roles in the development and malignant progression of human cancers. miR-148a has previously been found to inhibit the migration and invasion of breast cancer cells. However, the underlying mechanism of miR-148a in regulating the viability and migration of estrogen receptor (ER) α-positive breast cancer cells is still unknown. In this study, ERα-positive breast cancer MCF7 cells were treated with estradiol (E2). Data from MTT and wound healing assays showed that E2 treatment promoted the viability and migration of MCF7 cells. A bioinformatics analysis and luciferase reporter assay identified ERα as a direct target of miR-148a. Ectopic expression of miR-148a significantly decreased the protein expression of ERα (P&lt;0.01), while knockdown of miR-148a significantly increased the ERα protein level in MCF7 cells (P&lt;0.01). Furthermore, miR-148a overexpression significantly inhibited the E2-induced viability and migration of MCF7 cells (P&lt;0.01), similar to the effect of silencing ERα. However, overexpression of ERα rescued the suppressed viability and migration caused by miR-148a upregulation. Finally, it was found that E2 treatment led to a significant decrease in the miR-148a level in MCF7 cells (P&lt;0.01). These results suggest that miR-148a can suppress the E2-induced viability and migration of MCF7 breast cancer cells via inhibition of ERα protein expression, expanding the understanding of miR function in ERα-positive breast cancer. 

Retracted: No

PubPeer comments:
 Fig 3C,D.  Western blot analysis ... used to evaluate the protein ... expression of ERu03b1 . ![file] Light green box emphasises a band shared with Fig 3F of [Liu et al (2017)] ,  Western blot was used to examine the protein levels of ... MMP9 . ![file] , 
 Fig 4C.  MCF7 cells were transfected with ERu03b1u2011specific siRNA, and western blot analysis was used to evaluate the protein expression of ERu03b1. ![file] Pink box marks a matching band in [below] Figs 4C D from [Zhou et al (2016b)] .  Western blot was used to examine the protein levels of EMT-related genes . ![file] Also in Fig 7 from [Dai et al (2016)] .  Western blotting was performed to examine the (A) phosphorylated JNK (p-JNK) and total JNK (t-JNK), (B) phosphorylated ERK (p-ERK) and total ERK (t-ERK), (C) phosphorylated p38 (p-p38) MAPK and total p38 (t-p38) MAPK in the U87 cells transfected with the pcDNA3.1-CXCL5 plasmid or a blank vector as the negative control (NC), respectively. ![] , 
 *[left]* Fig 5A.  MCF7 cells were co-transfected with miR-148a mimic and ERu03b1 ORF plasmid, and western blot analysis was used to evaluate the protein expression of ERu03b1. *[right]* Fig 3A from [Su et al (2017)] .  Western blot ... conducted to detect the protein ... expression of p21 in HeLa cells transfected with ... NC inhibitor, and miR-92a inhibitor . ![file] ,