MiR-143 and MiR-145 regulate IGF1R to suppress cell proliferation in colorectal cancer
Authors: Wenjing Pang
Weiyan Yao
Xi Chen
Xueliang Wang
Hui Feng
Chihao Zhao
Zhen Fu
Ke Zen
Yanbo Wang
Nan Wang
Junfeng Zhang
Yanqing Liu
Hongwei Liang
Suyang Zhang
Xin Yan
Jiaojiao Su
Yalei Wang
Chen-Yu Zhang
Journal: PloS one (2014)
Discipline: Multidisciplinary
Keywords: Insulin-like growth factor 1 receptor; IGF1R; miRNAs; miR-143; miR-145
Affiliations: Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, China., Jiangsu Engineering Research Center for microRNA Biology and Biotechnology, State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, 22 Hankou Road, Nanjing, Jiangsu 210093, China., Department of Gastroenterology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China., The Comprehensive Cancer Center of Drum Tower Hospital affiliated to Medical School of Nanjing University & Clinical Cancer Institute of Nanjing University, Nanjing, Jiangsu 210008, China.

Abstract:  Insulin-like growth factor 1 receptor (IGF1R) is a transmembrane receptor that is activated by insulin-like growth factor 1 (IGF-1) and by a related hormone called IGF-2. It belongs to the large class of tyrosine kinase receptors and plays an important role in colorectal cancer etiology and progression. In this study, we used bioinformatic analyses to search for miRNAs that potentially target IGF1R. We identified specific target sites for miR-143 and miR-145 (miR-143/145) in the 3'-untranslated region (3'-UTR) of the IGF1R gene. These miRNAs are members of a cluster of miRNAs that have been reported to exhibit tumor suppressor activity. Consistent with the bioinformatic analyses, we identified an inverse correlation between miR-143/145 levels and IGF1R protein levels in colorectal cancer tissues. By overexpressing miR-143/145 in Caco2, HT29 and SW480 colorectal cancer cells, we experimentally validated that miR-143/145 directly recognizes the 3'-UTR of the IGF1R transcript and regulates IGF1R expression. Furthermore, the biological consequences of the targeting of IGF1R by miR-143/145 were examined by cell proliferation assays in vitro. We demonstrated that the repression of IGF1R by miR-143/145 suppressed the proliferation of Caco2 cells. Taken together, our findings provide evidence for a role of the miR-143/145 cluster as a tumor suppressor in colorectal cancer through the inhibition of IGF1R translation. 

Retracted: No

PubPeer comments:
 Similarities have been noted between panels in Figures 1 and 3 of this paper, and Figures 1 and 3 of another paper by the same authors, i.e. Zhongpu Chen, Xiaodong Pan, Yuyu Yao, Fengdi Yan, Long Chen, Rong Huang, Genshan Ma, Epigenetic Regulation of Cardiac Progenitor Cells Marker c-kit by Stromal Cell Derived Factor-1a, tPLOS ONE, July 2013 | Volume 8 | Issue 7 | e69134, doi:10.1371 journal.pone.0069134, https: pubpeer.com publications 644C2DECDE606242B2920FCF0397B1 The PLOS ONE paper got retracted today, February 12, 2021 for these similarities. Both papers also appear to have image duplications within their respective Figures 3C. Here as some illustrations of the noted similarities: ![file] ![file] I reported the image overlap highlighted with blue boxes to this journal in 2014, but it did not get addressed. ,