microRNA-141 inhibits cell proliferation and invasion and promotes apoptosis by targeting hepatocyte nuclear factor-3β in hepatocellular carcinoma cells
Authors: Xi Chen
Li Lin
Hongwei Liang
Tingyu Ren
Yanwei Hu
Hui Xu
Lei Zheng
Yanbo Wang
Jinlan Huang
Xiaomao Yin
Journal: BMC Cancer (2014)
Discipline: CLINICAL MEDICINE
Keywords: Hepatocyte nuclear factor-3β; HNF-3β; microRNAs; miRNAs; gene expression
Affiliations: Department of Laboratory Medicine, Nanfang Hospital, Southern Medical University, North of Guangzhou avenue No,1838, Baiyun District, Guangzhou 510515, P,R, China. .

Abstract:  Background: Hepatocyte nuclear factor-3β (HNF-3β) plays a critical role in hepatocyte differentiation and controls liver-specific gene expression during the development of hepatocellular carcinoma (HCC), but the molecular basis of this process has not been fully elucidated. microRNAs (miRNAs) are powerful, post-transcriptional regulators of gene expression. Whether miRNAs can impact the effects of HNF-3β in HCC is still unknown. Methods: HNF-3β and miR-141 expression levels were detected in HepG2 cells, using real-time quantitative RT-PCR (qRT-PCR). Luciferase reporter assays and Western blots were used to validate HNF-3β as a direct target gene of miR-141. Cell proliferation, invasion, and apoptosis were also examined to confirm whether miR-141 could impact on HNF-3β in HCC. Results: In this study, we found that HNF-3β protein levels were consistently upregulated in HCC clinical tissues compared with matched normal adjacent tissues. However, the mRNA levels of HNF-3β varied in random tissues, suggesting that a post-transcriptional mechanism was involved in its regulation. We used bioinformatic analyses to search for miRNAs that could potentially target HNF-3β, and identified specific targeting sites for miR-141 in the 3'-untranslated region (3'-UTR) of the HNF-3β gene. By overexpressing miR-141 in HepG2 cells, we experimentally validated that miR-141 directly regulated HNF-3β expression. Furthermore, the biological consequences of targeting HNF-3β by miR-141 were examined using cell proliferation, invasion and apoptosis assays in vitro. We demonstrated that the repression of HNF-3β by miR-141 suppressed the proliferation and invasion and promoted the apoptosis of HepG2 cells. Conclusions: miR-141 functions as a tumor suppressor in HCC cells through the inhibition of HNF-3β translation. 

Retracted: No

PubPeer comments:
 Figure 4A appears to have two images which overlap, at different magnification. *** ![file] , 
 #1 Dear Actinopolyspora Biskrensis, We sincerely apologize for this mistake in our article. First of all, we promise that all of the experimental data are true and credible. We have checked the raw data of Figure 4A (please see the image below) and found that the mistake was made when we assembled different panels of Figure 4A. We collected low resolution and high resolution images for each transwell assay. At first, we planned to use the high resolution images; however, it seemed that the low resolution images might display more clearly the whole picture of migrant cells. Therefore, we decided to replace the high resolution images with low resolution images. Unfortunately, the high resolution image of the u201ccontrol plasmidu201d group was omitted and accidentally placed in the position of the u201cpre-miR-control+control plasmidu201d group. We apologize for not checking it out. We will contact the journal to explain what has happened and send a new version of Figure 4A to address this issue. The corrected figure does not affect the interpretation or conclusions of this paper. We sincerely apologize to our readers for any confusion this unintentional error might have caused.![file] , 
 Thank you for addressing this. It is concerning that this group seems to have [multiple papers] with similar image issues. ,