microRNA-98 inhibits the proliferation, invasion, migration and promotes apoptosis of breast cancer cells by binding to HMGA2
Authors: Mi-Jia Wang
Hai-Dong Zhao
Jun Li
Hao Zhang
Journal: Bioscience Reports (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Breast cancer; High mobility group AT-hook 2; Invasion; Migration; Proliferation
Affiliations: Department of Breast Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian 116000, P.R. China., Department of Breast Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian 116000, P.R. China .

Abstract:  Breast cancer is a major contributor leading to cancer death in females worldwide. The aim of the present study was to investigate the effects of microRNA-98 (miR-98) on the processes of cell proliferation, invasion, migration and apoptosis by binding to high-mobility group AT-hook 2 (HMGA2) in breast cancer. Breast cancer tissues and adjacent normal tissues were collected from 112 patients suffering from breast cancer. The target relationship between miR-98 and HMGA2 was verified by in connection with the bioinformatics website as well as a dual-luciferase reporter assay, both of which provided evidence indicating that HMGA2 was a target gene of miR-98. Human breast cancer MDA-MB-231 cells were treated with miR-98 mimics, miR-98 inhibitors, siRNA-HMGA2 or miR-98 inhibitors + siRNA-HMGA2. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry methods were performed to determine cell proliferation, cell cycle and apoptosis, respectively, while a Transwell assay was employed to detect cell migration and invasion. Breast cancer tissues exhibited decreased miR-98 expression, while increased expression levels of HMGA2 were recorded. The mRNA and protein expressions of HMGA2, cell proliferation, cells at the S phase, cell migration, invasion, expressions of matrix metalloproteinase (MMP)2 as well as MMP9 were all reduced in response to miR-98 mimics or siRNA-HMGA2, while a contradictory trend was observed in the miR-98 inhibitors group. In conclusion, the results of the study demonstrate that miR-98 inhibits cell proliferation, migration and invasion, while acting to promote apoptosis by negatively regulating HMGA2 in breast cancer. 

Retracted: No

PubPeer comments:
 Fig 4B.  (B) Protein bands of HMGA2 protein expression in human breast cancer MDA-MB-231 cells after transfection, determined by Western blot assay. ![file] The loading control is distinctive (especially the bubble beneath one of the bands), and occurs in a number of papers from otherwise-unrelated teams of authors, creating the unfortunate suspicion that this paper is a product of the  contractor papermill, [discussed in blogposts] . Other examples are itemised in [a Google Document] . Compare, for instance, the loading control from 7B of [Zhou et al (2018)] . ![file] Figs 2C, 4C, 10D from [Yan et al (2017)] . ![file] , 
 Fig 6  (A) Cell cycle detected by flow cytometry. ![file] Overhangs in a cell-count histogram create concerns that it was hand-drawn. , 
 The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. , 
 Figures 7A and 7C want to join in, with overlapping images (sometimes after flipping) and some contrast adjustments. *** ![file] , 
 Retracted [8 June 2021] . ----------------------------------- This Retraction follows an Expression of Concern relating to this article previously published by Portland Press. This article is being retracted from Bioscience Reports at the request of the Editor-in-Chief and the Editorial Board following receipt of a notification from a reader, alerting the Editorial Board to the Western blots in Figure 4B which are duplicated in several other publications, as well as duplications in Figures 7A and 7C. The authors have been contacted in regards to the retraction, and have not responded to the Journal s queries and the concerns raised. Given the extent of the issues raised, the Editorial Board stand by the decision to retract the article. ,