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Zhu X, Luo W, Liang W, et al. Onco Targets Ther.  2016;9:7493— 7501. The Editor-in Chief and Publisher of OncoTargets and Therapy wish to retract the published article. Concerns were raised that images shown in Figure 4A of the published article appeared to have been duplicated with images shown in Figure 2d of the article ‘Correlations between chromobox homolog 8 and key factors of epithelial–mesenchymal transition in hepatocellular carcinoma’ published in Cancer Cell International (https://doi.org/10.1186/s12935-019-1063-z). Specifically, it appears the following images may have been duplicated:● Figure 4A PANC-1 Invasion shGFP appears duplicated with Figure 2d SK-Hep-1 Invasion shCBX8-3#● Figure 4A PANC-1 Migration shGFP appears duplicated with Figure 2d SK-Hep-1 Invasion shGFP● Figure 4A PANC-1 Migration shMAZ-2# appears duplicated with Figure 2d SK-Hep-1 Invasion shCBX8-1# The editor was concerned the articles were published three years apart and the article published in OncoTargets and Therapy described a study investigating pancreatic carcinoma, while the article published in Cancer Cell International described a study investigating hepatocellular carcinoma. There were also concerns it appeared the same images were used to show results for two different cell lines, PANC-1 and SK-Hep-1. The authors could not provide a satisfactory explanation for why it appeared the same images had been used to show results from two different cell lines. The authors were also unable to provide satisfactory raw data for their study and the editor determined the studies finding were no longer valid.    The authors wish to apologise for this error. Our decision-making was informed by our policy on publish

Shidong Zhang,1,* Run Tian,1,* Chunhua Bei,1 Huixia Zhang,1 Juan Kong,1 Chuanjun Zheng,1 Xin Song,1 Di Li,1 Hongzhuan Tan,2 Xiaonian Zhu,1 Shengkui Tan1,2 1Department of Epidemiology and Health Statistics, School of Public Health, Guilin Medical University, Guilin 541199, Guangxi, People’s Republic of China; 2Department of Epidemiology and Health Statistics, School of Public Health, Central South University, Changsha 410005, People’s Republic of China*These authors contributed equally to this workCorrespondence: Shengkui Tan; Xiaonian Zhu Email sktan2008@163.com; zhuxiaonian0403@163.comBackground: Our recent study identified that human chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family member 2 (CMTM2) was deregulated in hepatocellular carcinoma (HCC) tissues and posed as a potential tumor suppressor. However, the mechanism of CMTM2 in HCC occurrence and development has not been well elaborated.Materials and Methods: The expression of CMTM2 was knocked-down by RNA interruption in Huh-7 and SMMC7721 cells. Cell proliferation ability was detected by CCK8 test and colony formation assay. The cell invasion and migration were measured by wound healing and Transwell assay.Results: We found that the cell proliferation was significantly increased by interruption of CMTM2 expression, both in Huh-7 and SMMC7721 cells. Moreover, down-regulated CMTM2 could promote the invasion and migration ability of HCC cells through inducing the epithelial-mesenchymal transition (EMT) process. We further discovered that both the expression of CMTM2 and the EMT-associated marker E-cadherin were decreased in the same thirty cases of HCC tissues compared with the corresponding adjacent non-tumor tissues. Pearson correlation test showed that there was a significantly positive correlation between CMTM2 and E-cadherin in HCC tissues (P< 0.05).Conclusion: Based on the results of cell model and HCC tissues, our study suggests that down-regulate

Chunhua Bei,1,* Ying Zhang,1,* Riming Wei,1 Xiaonian Zhu,1 Zhigang Wang,1 Wen Zeng,2 Qiuyue Chen,3 Shengkui Tan1 1Department of Epidemiology and Statistics, School of Public Health, Guilin Medical University, 2Department of Hepatobiliary Surgery, The Affiliated Hospital of Guilin Medical University, 3Department of Pathology, 181st Hospital of Chinese People’s Liberation Army, Guilin, People’s Republic of China *These authors contributed equally to this work Abstract: CMTM4 is the most conserved member of chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing (CMTM) family on chromosome 16q22.1, a locus that harbors a number of tumor-suppressor genes. In previous studies, CMTM4 was reported to be downregulated and exhibited tumor-suppressor activities by regulating cell growth and cell cycle in clear cell renal cell carcinoma. However, its roles in tumorigenesis of hepatocellular carcinoma (HCC) remain poorly studied. This study first investigated the expression of CMTM4 in HCC, and then examined the association between the expression of CMTM4 with the clinicopathological features and prognosis of HCC patients. It was found that CMTM4 was downregulated in HCC tissues, compared with matched adjacent nontumor tissues, as detected by immunohistochemistry. In addition, Kaplan–Meier survival analysis showed that the negative expression of CMTM4 was associated with decreased overall survival rates in patients with HCC. The results of this study suggest CMTM4 plays a role as a tumor suppressor in HCC and CMTM4 negative expression is a risk factor for poor prognosis of HCC. Keywords: chemokine-like factor-like MARVEL transmembrane domain-containing 4, hepatocellular carcinoma, immunohistochemistry, prognosis

This paper has been retracted.Xiaonian Zhu, 1,* Wei Luo, 2,* Wenjin Liang, 2 Fen Tang, 3 Chunhua Bei, 1 Yuan Ren, 1 Linyuan Qin, 1 Chao Tan, 1 Ying Zhang, 1 Shengkui Tan 1 1School of Public Health, Guilin Medical University, Guilin, People’s Republic of China; 2Department of Hepatobiliary Surgery, The Affiliated Hospital of Guilin Medical University, Guilin, People’s Republic of China; 3Department of Hepatology, Nanxishan Hospital of Guangxi Zhuang Autonomous Region, Guilin, People’s Republic of China *These authors contributed equally to this work Abstract: This study aimed to investigate the expression and clinical significance of MYC-associated zinc finger protein (MAZ) in pancreatic carcinoma (PC), and the biological functions of MAZ in PC cells. MAZ expression was detected in 57 PC tissues and 41 paired adjacent nontumor tissues by immunohistochemistry. Compared to the expression in adjacent nontumor tissues, MAZ was significantly higher expressed in PC tissues (P< 0.0001). In addition, MAZ expression had a significant correlation with certain clinical characteristics of PC patients, such as age, tumor diameter, tumor number, and the serum level of CA199 (P< 0.05). The survival analysis showed that the survival time of PC patients with high expression of MAZ was significantly lower than patients with low expression of MAZ (P=0.0365). After MAZ was knocked down in PANC-1 cells by RNA interference, the cells’ ability to proliferate, invade, and migrate was decreased significantly (P< 0.01). Moreover, MAZ expression was found to be associated with Ki-67, a cell proliferation marker, in PC tissues, further supporting the idea that MAZ promotes PC cell proliferation. Our study clarifies an oncogenic role of MAZ in pathogenesis of PC and provides MAZ as a biomarker in the treatment and prognosis of PC. Keywords: pancreatic carcinoma, MYC-associated zinc finger protein, prognosis, cell proliferation