Search

Song X, Xu X, Ren X, Ruan X, Wang Y, Yao TT. Onco Targets Ther. 2020;13:8907–8917 At the authors request, the Editor and Publisher of OncoTargets and Therapy are retracting the published article. The authors found errors in the article, including the duplication of images in Figure 3. Specifically, The image used for Figure 3A, HCCLM3, Vector, was duplicated with the image for Figure 3B, HCCLM3, Control. The authors informed the journal that they were unable to provide adequate data to verify the findings and requested a retraction. The editor agreed with this decision. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”.

Xue-zhen Song,1 Xiao-jun Xu,1 Xiao-ning Ren,1 Xiao-xuan Ruan,1 Yi-li Wang,2 Ting-Ting Yao1 1Department of Blood Transfusion, Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University, Weihai, Shandong, People’s Republic of China; 2Department of Hematology, Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University, Weihai, Shandong, People’s Republic of ChinaCorrespondence: Xue-zhen Song Email sxm115578@126.comObjective: Our study aimed to investigate the effect of anti-differentiation noncoding RNA (ANCR) on hepatocellular carcinoma (HCC) and its potential molecular mechanisms.Methods: The expression of ANCR was detected by qRT-RCR in both HCC tissues and HCC cells. Moreover, the relationship between ANCR expression and clinical parameters in HCC patients was investigated. The proliferation, cell clones, migration, invasion and apoptosis of MHCC97H and HCCLM3 cells were measured by MTT assay, colony formation assay, transwell assay and flow cytometry, respectively. The expressions of N-cadherin, vimentin, E-cadherin, cleaved caspase-3, Bax, Bcl-2, Wnt1, β-catenin and GSK-3β in MHCC97H and HCCLM3 cells were measured by Western blot.Results: Our results showed that ANCR was lowly expressed in both HCC tissues and HCC cells. ANCR expression was closely associated with tumor size, tumor-node-metastasis (TNM) stages and vascular invasion in HCC. ANCR could dramatically inhibit cell proliferation, migration and invasion, as well as promote apoptosis in MHCC97H and HCCLM3 cells. ANCR could significantly increase the expression of cleaved caspase-3, Bax, E-cadherin and GSK-3β but reduce the expression of Bcl-2, N-cadherin, vimentin, Wnt1 and β-catenin in MHCC97H and HCCLM3 cells. In addition, Wnt/β-catenin pathway inhibitor (IWP-2) partially reversed the effects of silencing ANCR on the proliferation, migration, invasion and apoptosis of HCCLM3 cells.Conclusion: Our study demonstrated that ANCR can suppress cell proliferation, migration and invasion, as well as promote apoptosis of HCC cells via modulation of the Wnt/β-catenin signaling pathway.Keywords: hepatocellular carcinoma, ANCR, proliferation, apoptosis, metastasis, Wnt/β-catenin pathway

Objective Our study aimed to investigate the effect of anti-differentiation noncoding RNA (ANCR) on hepatocellular carcinoma (HCC) and its potential molecular mechanisms. Methods The expression of ANCR was detected by qRT-RCR in both HCC tissues and HCC cells. Moreover, the relationship between ANCR expression and clinical parameters in HCC patients was investigated. The proliferation, cell clones, migration, invasion and apoptosis of MHCC97H and HCCLM3 cells were measured by MTT assay, colony formation assay, transwell assay and flow cytometry, respectively. The expressions of N-cadherin, vimentin, E-cadherin, cleaved caspase-3, Bax, Bcl-2, Wnt1, β-catenin and GSK-3β in MHCC97H and HCCLM3 cells were measured by Western blot. Results Our results showed that ANCR was lowly expressed in both HCC tissues and HCC cells. ANCR expression was closely associated with tumor size, tumor-node-metastasis (TNM) stages and vascular invasion in HCC. ANCR could dramatically inhibit cell proliferation, migration and invasion, as well as promote apoptosis in MHCC97H and HCCLM3 cells. ANCR could significantly increase the expression of cleaved caspase-3, Bax, E-cadherin and GSK-3β but reduce the expression of Bcl-2, N-cadherin, vimentin, Wnt1 and β-catenin in MHCC97H and HCCLM3 cells. In addition, Wnt/β-catenin pathway inhibitor (IWP-2) partially reversed the effects of silencing ANCR on the proliferation, migration, invasion and apoptosis of HCCLM3 cells. Conclusion Our study demonstrated that ANCR can suppress cell proliferation, migration and invasion, as well as promote apoptosis of HCC cells via modulation of the Wnt/β-catenin signaling pathway.