Overexpression of HES6 has prognostic value and promotes metastasis via the Wnt/β-catenin signaling pathway in colorectal cancer
Authors: Huizhong Zhang
Yuandong Xu
Ziyuan Zhu
Shuling Li
Xiaobing Wu
Xuehu Xu
Xuejuan Liu
Libing Song
Xianqiu Wu
Journal: Oncology Reports (2018)
Discipline: CLINICAL MEDICINE
Keywords: HES6; colorectal cancer; oncogenesis; cancer progression; prognosis
Affiliations: Department of Gastrointestinal Surgery, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510150, P.R. China., Department of Pathology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, Guangdong 510060, P.R. China., Department of Experimental Research, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong 510060, P.R. China.

Abstract:  HES6 is a member of the hairy-enhancer of the split homolog family, which has been implicated in oncogenesis and cancer progression in a variety of human cancers, including prostate and breast cancer. However, its clinical significance and biological role in colorectal cancer (CRC) remain unclear. In the present study, the expression of HES6 was significantly upregulated in CRC cell lines and CRC tissues at both the mRNA and protein levels. The present study also reported high expression of HES6 in 138/213 (64.8%) paraffin-embedded archived CRC specimens. HES6 expression was significantly correlated with T classification (P&lt;0.001), N classification (P=0.020), and distant metastasis (P&lt;0.001). Patients with higher HES6 expression levels exhibited a reduced overall survival (P&lt;0.001). In addition, a multivariate analysis revealed that the expression of HES6 may be a novel prognostic marker for the survival of patients with CRC. Furthermore, the present study demonstrated that ectopic expression of HES6 enhanced the migration and invasive abilities of CRC cells. These abilities were significantly inhibited upon knockdown of endogenous HES6 expression by specific short hairpin RNAs. Additionally, the present study reported that the effects of HES6 on metastasis may be associated with the activation of the Wnt/β-catenin signaling pathway. Collectively, the findings of the present study revealed that overexpression of HES6 played a key role in the progression of CRC, leading to a poor prognosis and clinical outcome. 

Retracted: No

PubPeer comments:
 Figure 2D appears to have 2 images which overlap. This is sometimes seen in papermill products. See also: https: pubpeer.com search?q=authors%3A%22Libing+Song%22 *** ![file] , 
 Figure 5D and 8A also appear to have an image which overlaps. Could the authors please check? *** ![file] , 
 Dear Actinopolyspora Biskrensisuff1a Thanks for pointing this out. We are currently checking the original data of these Figures, and will make response as soon as possible. Xuehu Xu , 
 Corrigendum, [23 March 2022] . ---------------------- Subsequently to the publication of the above article, an interested reader drew to the authors attention that Fig. 2 on p. 1266 and Fig. 5 on p. 1269 contained some apparent errors in terms of the assembly of the various data panels. Specifically, Fig. 2D appeared to contain a pair of overlapping images, and Figs. 5D and 8A also appeared to include overlapping images. However, the authors were able to consult their original data, and assess where the errors had been made during the compilation of these figures. The corrected versions of Figs. 2 (showing the correct data for the u20185Tu2019 panel in Fig. 2D) and 5 (showing alternative data) are shown on the subsequent pages. The authors regret the errors that were made during the preparation of the published figures, and confirm that these errors did not grossly affect the conclusions reported in the study. The authors are grateful to the Editor of *Oncology Reports* for allowing them the opportunity to publish a Corrigendum, and all the authors agree to this Corrigendum. Furthermore, they apologize to the readership for any inconvenience caused. ,