MiR-143-3p functions as a tumor suppressor by regulating cell proliferation, invasion and epithelial-mesenchymal transition by targeting QKI-5 in esophageal squamous cell carcinoma
Authors: Haizhu Song
Jun Yi
Jing Chen
Siqi Han
Zhenyue He
Xiaolong Liu
Longbang Chen
Li Jin
Journal: Molecular Cancer (2016)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Esophageal squamous cell carcinoma; Invasion; MiR-143-3p; Proliferation; QKI-5.
Affiliations: Department of Medical Oncology, Jinling Hospital, Medical School of Nanjing University, 305 Zhongshan East Road, Nanjing, Jiangsu, 210002, People's Republic of China., Department of Cardiothoracic Surgery, Jinling Hospital, Medical School of Nanjing University, 305 Zhongshan East Road, Nanjing, Jiangsu, 210002, People's Republic of China., Department of Medical Oncology, Jinling Hospital, Medical School of Nanjing University, 305 Zhongshan East Road, Nanjing, Jiangsu, 210002, People's Republic of China. .

Abstract:  Background: Dysregulation of microRNAs (miRNAs) have been demonstrated to contribute to carcinogenesis. MiR-143-3p has been identified to function as a tumor suppressor in several tumors, but the role of miR-143-3p in esophageal squamous cell carcinoma (ESCC) has not been intensively investigated. Our aim was to evaluate the potential role of miR-143-3p in the progression of ESCC. Methods: The expression levels of miR-143-3p and QKI-5 protein were measured in 80 resected ESCC tumor specimens and the clinicopathological significance of these levels determined. We also investigated the role of miR-143-3p in the regulation of QKI-5 expression in ESCC cell lines both in vivo and in vitro. Results: MiR-143-3p levels were decreased in ESCC clinical samples and low expression of miR-143-3p was significantly associated with poor prognosis in ESCC patients. Ectopic expression of miR-143-3p suppressed proliferation and induced apoptosis in ESCC cells both in vivo and in vitro. Ectopic expression of miR-143-3p also reduced the metastatic potential of cells by selectively regulating epithelial-mesenchymal transition regulatory proteins. Furthermore, QKI-5 isoform was upregulated in ESCC tissues and was a direct target of miR-143-3p. Lastly, re-introduction of QKI-5 expression abrogated the inhibitory effects of miR-143-3p on ESCC cell proliferation and motility. Conclusions: Our results demonstrate that miR-143-3p acts as a tumor-suppressor by targeting QKI-5 in ESCC, suggesting that miR-143-3p is a potential therapy for the treatment of ESCC. 

Retracted: No

PubPeer comments:
 Figure 3, 6, and 7 appear to have some image duplications ![file] ![file] ![file] There could be more. , 
 #1 You were right. I identified one additional overlap from 6 and 7 in yellow (approximate location), but looked no further. Note there seems to be a white feature in Figure 6 that does not appear in 7. *** ![file] , 
 Figure 8 has similar issues. I alerted the journal today. *** ![file] , 
 Retracted, [24 August 2022] .  The Editor in Chief has retracted this article because of significant concerns regarding a number of Figures presented in this work, which question the integrity of the data. The Editor-in-Chief therefore no longer has confidence in the integrity of the data in this article. All authors agree to this retraction. ,