Hypoxia-induced lncRNA EIF3J-AS1 accelerates hepatocellular carcinoma progression via targeting miR-122–5p/CTNND2 axis
Authors: Tianxiang Chen
Yongshen Niu
Bowen Yao
Cheng Guo
Liang Wang
Demao Yao
Huanye Mo
Xue Yang
Journal: Biochemical and biophysical research communications (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: CTNND2; EIF3J-AS1; Hepatocellular carcinoma; Tumor progression; miR-122–5p.
Affiliations: Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi Province, 710061, China., Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi Province, 710061, China. Electronic address: ., Department of Geriatric Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi Province, 710061, China. Electronic address: .

Abstract:  Long noncoding RNAs (lncRNAs) exert crucial roles in hepatocellular carcinoma (HCC) progression. LncRNA EIF3J-AS1 is recently reported to be highly expressed in HCC and correlates with recurrence-free survival. However, the biological function of EIF3J-AS1 and its underlying molecular mechanism are unexplored yet. In the current study, we demonstrated that EIF3J-AS1 expression was obviously upregulated in HCC tissues compared to adjacent noncancerous tissues. Moreover, the elevated levels of EIF3J-AS1 was detected in four HCC cell lines (HepG2, SMMC-7721, MHCC97H, HCCLM3) compared with the normal hepatic cell line LO2. Notably, the expression of EIF3J-AS1 was correlated with prognostic features including tumor size, vascular invasion and tumor stage. TCGA-LIHC data indicated that the upregulated expression of EIF3J-AS1 predicted poor prognosis of HCC. EIF3J-AS1 knockdown remarkably suppressed the proliferation, migration and invasion of HCC cells. Mechanistically, EIF3J-AS1 inversely regulated miR-122-5p expression via acting as a competing endogenous RNA (ceRNA) in HCC cells. Furthermore, catenin delta 2 (CTNND2) was recognized as a novel target of miR-122-5p. CTNND2 restoration partially reversed EIF3J-AS1 knockdown-induced inhibitory effects on HCC cell proliferation, migration and invasion. Importantly, we found that hypoxia induced EIF3J-AS1 and CTNND2 expression, and led to miR-122-5p downregulation in HCC cells. EIF3J-AS1 knockdown partially abolished hypoxia-induced HCC cell proliferation and mobility. In conclusion, our results provide a new insight into the molecular pathogenesis of HCC, and EIF3J-AS1 may be a potential therapeutic target for HCC. 

Retracted: No

PubPeer comments:
 Figure 2D. * Blue boxes. Two panels appear to show an overlap ![file] , 
 A hard-to-find Correction, published online May 2021, found here: https: www.sciencedirect.com science article pii S0006291X21007294  In our paper [1], two images (migrated MHCC97H cells with EIF3J-AS1 knockdown) in Fig. 2D were mistakenly uploaded in the original publication. Through repeated confirmation, we captured the images of migrated MHCC97H cells with EIF3J-AS1 knockdown at the same time and confirmed that we mistakenly attached two images in Fig. 2D due to the negligence. Because shEIF3J-AS1-1 and shEIF3J-AS1-2 had the same effects on the migration ability of MHCC97H cells, we confirmed that this mistake in Fig. 2D did not affect the research results and conclusion of this article. All authors have agreed to this corrigendum, and we apologize for the negligence in our work and hope to get the opportunity to correct this mistake. Fig. 2D should be corrected as follows. ,