<p>LINC02476 Promotes the Malignant Phenotype of Hepatocellular Carcinoma by Sponging miR-497 and Increasing HMGA2 Expression</p>
Authors: Yuxia Duan
Mengjing Zhao
Zhi Li
Caifang Ni
Mengmeng Jiang
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: HMGA2; LINC02476; hepatocellular carcinoma; miR-497.
Affiliations: Department of Interventional Radiology, The First Affiliated Hospital of Soochow University, Suzhou 215006, People's Republic of China., Department of Radiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, People's Republic of China.

Abstract:  Background: Long noncoding RNAs (lncRNAs) can promote hepatocellular carcinoma (HCC) initiation and progression. In this report, we examined the role of lncRNA LINC02476 in HCC. Methods: The expression levels of different lncRNAs in HCC were explored using the TCGA database and lncRNA LINC02476 was selected for further study. The expression of LINC02476 in HCC tissues was determined by real-time PCR. The clinicopathological characteristics of HCC patients were analyzed relative to the expression of LINC02476. The expression of LINC02476 was downregulated in HCC cells using a lentiviral vector and different assays were performed to study cell growth, proliferation, invasion, apoptosis and the cell cycle. MiR-497 was selected as a miRNA that could interact with LINC02476 which was further tested by RNA immunoprecipitation. HMGA2 was selected as a possible target of miR-497, and their interaction was examined by a luciferase reporter assay. Results: LINC02476 expression was elevated in HCC cell lines and HCC tissues. When LINC02476 was downregulated, the growth and the invasion of HCC cells decreased in vitro and in vivo. LINC02476 negatively regulated the expression of miR-497 by acting as a ceRNA. HMGA2 was directly targeted and inhibited by miR-497. Conclusion: The results indicate that LINC02476 functions through the miR-497/HMGA2 axis and that it has a role in the growth and metastasis of HCC cells. Therefore, LINC02476 could be an interesting new molecular target in HCC therapies. 

Retracted: Yes

PubPeer comments:
null, 
 Original figure 3B. Not whole lanes duplicated, but parts of lanes, parts of bands duplicated. , 
 ![image] , 
 https: retractionwatch.com 2014 01 06 fourth-retraction-results-from-cardiff-investigation , 
 Figure 1B. Much more similar than expected. ![file] , 
 #3 Refinement of figure 3B. ![file] , 
 17 Nov 2021 Retraction. Retraction notice. https: academic.oup.com nar advance-article doi 10.1093 nar gkab1151 6426056 Retraction of u2018Interplay between REST and nucleolin transcription factors: a key mechanism in the overexpression of genes upon increased phosphorylationu2019 Nucleic Acids Research, gkab1151, https: doi.org 10.1093 nar gkab1151 Published: 17 November 2021 Nucleic Acids Research, Volume 38, Issue 9, 1 May 2010, Pages 2799u20132812, https: doi.org 10.1093 nar gkq013 Following allegations of image manipulation in Figure 3B of the above article (1) a corrigendum was published in 2014 (2). After allegations of image manipulation in Figure 1B were raised in 2021, the Editors of Nucleic Acids Research investigated again and are now retracting the article after having determined Lane 2 has been altered by partly copying Lane 1 and manually adding some bands. According to COPE guidelines , the Editors are therefore retracting the article from Nucleic Acids Research and have informed the institution. REFERENCES 1.tTediose T., Kolev M., Sivasankar B., Brennan P., Morgan B.P., Donev R. Interplay between REST and nucleolin transcription factors: a key mechanism in the overexpression of genes upon increased phosphorylation. Nucleic Acids Res. 2010; 38:2799u20132812. 2.tTediose T., Kolev M., Sivasankar B., Brennan P., Morgan B.P., Donev R. Interplay between REST and nucleolin transcription factors: a key mechanism in the overexpression of genes upon increased phosphorylation. Nucleic Acids Res. 2014; 42:2798. ,