MicroRNA-503 inhibits the proliferation and invasion of breast cancer cells via targeting insulin-like growth factor 1 receptor
Authors: Taiping Du
Jingwang Yan
Haipeng Wang
Yonghuan Xu
Hao Chen
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; miR-503; breast cancer; proliferation; invasion
Affiliations: Department of General Surgery, Xinxiang Center Hospital, Xinxiang, Henan 453000, P.R. China., Department of Oncology, People's Hospital of Xixia County, Nanyang, Henan 474550, P.R. China.

Abstract:  MicroRNAs (miRs), a class of non-coding RNAs that are 18‚Ä?5 nucleotides in length, serve as key regulators in the development and progression of human cancers. Previously, miR‚Ä?03 has been implicated in breast cancer. However, the underlying mechanism of miR‚Ä?03 in regulating the proliferation and invasion of breast cancer cells remains largely unknown. In the present study, reverse transcription‚Äëquantitative polymerase chain reaction analysis indicated that the expression of miR‚Ä?03 was significantly reduced in breast cancer tissues compared with their matched adjacent normal tissues. Furthermore, miR‚Ä?03 expression levels were markedly reduced in T2‚ÄëT4 stage breast cancer, compared with T1 stage. Insulin‚Äëlike growth factor 1 receptor (IGF‚Ä?R) was further identified as a novel target of miR‚Ä?03. Overexpression of miR‚Ä?03 significantly suppressed the protein expression levels of IGF‚Ä?R. Furthermore, it inhibited the proliferation and invasion of human breast cancer MCF‚Ä? cells, as assessed by MTT and Transwell assays, respectively. However, restoration of IGF‚Ä?R expression markedly ameliorated the suppressive effects of miR‚Ä?03 overexpression on MCF‚Ä? cell proliferation and invasion, indicating that miR‚Ä?03 inhibits breast cancer cell proliferation and invasion at least partially via directly targeting IGF‚Ä?R. Furthermore, the mRNA and protein expression levels of IGF‚Ä?R were demonstrated to be significantly increased in breast cancer tissues compared with their matched adjacent normal tissues. In addition, IGF‚Ä?R mRNA expression levels were reversely correlated with miR‚Ä?03 expression levels in breast tumors, suggesting that the upregulation of IGF‚Ä?R may be due to downregulation of miR‚Ä?03 in breast cancer. In conclusion, the present study expanded the understanding of the regulatory mechanism of miR‚Ä?03 in breast cancer, and implicates the miR‚Ä?03/IGF‚Ä?R axis as a potential therapeutic target for breast cancer. 

Retracted: Yes

PubPeer comments:
  I set up a spreadsheet to include the various papers using this versatile suite of Transwell images to represent all possible combinations of cell-lines and treatments. This is the 38th manifestation. For comparison: Fig 3 C D from [Zhang et al (2016)] .  Transwell assay were performed to examine the migratory and invasive capacities of Saos-2 and U2OS cells transfected with miR-205 mimic or miR-negative control (NC) mimic , and Fig 7C D,  Transwell assay were performed to examine cell migration and invasion of MG63 or U2OS cells transfected with miR-205 mimic, or co-transfected with miR-205 mimic and RUNX2 plasmid .  Figs 4D, 6D from [Xia et al (2016)] .  Also *[above]* Fig 4C from [Lai, Chen Li (2015)] .  a Transwell assay were performed to examine the cell proliferation of AGS cells transfected with miR-133a mimics, miR-133a inhibitor, or co-transfected with miR-133a mimics and FSCN1 plasmid. Control: AGS cells without any transfection. *[below]* Figs 3(B), 6(B) from [Shi et al (2015)] .  Transwell assay was performed to determine the invasive capacity of the Saos-2 and U-2 OS cells transfected with NC scramble miRNA or miR-204 mimics, respectively. Control, Saos-2 and U-2 OS cells without any transfection ...  Transwell assay was performed to determine the invasive capacity of the Saos-2 and U-2 OS cells transfected with Sirt1 siRNA or co-transfected with miR-204 mimics and the Sirt1 plasmid, respectively. Control, Saos-2 and U-2 OS cells without any transfection .  , 
 Retracted [21 February 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 Fig. 4B and E 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 *Molecular Medicine Reports*, 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. ,