scholarly journals Retraction: MicroRNA-1271 modulates hepatitis B virus replication, cell proliferation and apoptosis in hepatitis B virus-related hepatocellular carcinoma by targeting SIRT1

RSC Advances ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 5698-5698
Author(s):  
Laura Fisher

Retraction of ‘MicroRNA-1271 modulates hepatitis B virus replication, cell proliferation and apoptosis in hepatitis B virus-related hepatocellular carcinoma by targeting SIRT1’ by Fei Tang et al., RSC Adv., 2019, 9, 39904–39913, DOI: 10.1039/C9RA08248D.

RSC Advances ◽  
2019 ◽  
Vol 9 (68) ◽  
pp. 39904-39913
Author(s):  
Fei Tang ◽  
Fengmei Wang ◽  
Hongmin Lv ◽  
Huiling Xiang ◽  
Yi Liu ◽  
...  

MiR-1271 suppressed HBV-related HCC cells development by downregulating SIRT1.


2011 ◽  
Vol 411 (3) ◽  
pp. 586-592 ◽  
Author(s):  
Chun-Mei Wang ◽  
Yan Wang ◽  
Chun-Guang Fan ◽  
Fei-Fei Xu ◽  
Wen-Sheng Sun ◽  
...  

2014 ◽  
Vol 92 (2) ◽  
pp. 152-162 ◽  
Author(s):  
Yanrui Sheng ◽  
Shijia Ding ◽  
Ke Chen ◽  
Juan Chen ◽  
Sen Wang ◽  
...  

MicroRNA-101(miR-101) has been shown to be down-regulated in hepatocellular carcinoma (HCC). The hepatitis B virus (HBV) is a major risk factor in the development and progression of HCC. However, the correlation between HBV and miR-101 has not yet been fully elucidated. In this study, we reported that HBV could repress miR-101-3p by inhibiting its promoter activity and identified the potential effects of miR-101-3p on some important biological properties of HCC cells by targeting Rap1b. Dual-luciferase reporter assays showed that HBV down-regulated miR-101-3p by inhibiting its promoter activity. Down-regulation of miR-101-3p promoted cell proliferation, migration, and reduced apoptosis, and resulted in up-regulation of Rap1b, while overexpression of miR-101-3p inhibited these processes. Moreover, overexpression of Rap1b was able to reverse the suppressed cell proliferation and migration mediated by miR-101-3p. Our data showed that HBV down-regulated miR-101-3p expression by inhibiting its promoter activity, which resulted in up-regulation of Rap1b, and down-regulation of miR-101-3p or up-regulation of Rap1b promoted proliferation and migration of HCC cells. This provides a new understanding of the mechanism of HBV-related HCC pathogenesis and the potential application of miR-101-3p in cancer therapy.


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