GALNT6 Promotes Tumorigenicity and Metastasis of Breast Cancer Cell via β-catenin/MUC1-C Signaling Pathway
Authors: Xiaoming Chen
Yingge Mao
Lili Tang
Sairong Fan
Yuqi Zhang
Jianxin Lyu
Lvao Chen
Journal: International Journal of Biological Sciences (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: GALNT6; glycosyltransferase; metastasis, β-catenin; proliferation.
Affiliations: Institute of Glycobiological Engineering, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China., Zhejiang Provincial Key Laboratory of Medical Genetics, Key Laboratory of Laboratory Medicine, Ministry of Education, China, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China., Present address: The First Affiliated Hospital of Henan University., Hangzhou Medical College, Hangzhou, Zhejiang, China.

Abstract:  Polypeptide N-acetylgalactosaminyl transferase-6 (GALNT6), a member of the N-acetyl-D-galactosamine transferase family, was shown to be over-expression in mammary cancer and could be used as a biomarker. However, its roles and underlying mechanisms in the pathogenesis of breast cancer are still unclear. In this study, we reported that GALNT6 was up-expression in breast cancer, and it was not associated with tumor stage. The expression level of GALNT6 and menopause status was associated with patient survival. Biological function results illustrated that knockdown of GALNT6 inhibited proliferation, migration and invasion of MDA-MB-231 cells, and increased cell apoptosis. Knockdown of GALNT6 in breast cancer cell attenuated the protein expression of PCNA, cyclin D1, C-myc and β-catenin, and increased the expression of E-cadherin, caspase 3 and cleaved PARP1. Cell fractionation assay showed that knockdown of GALNT6 reduced the levels of β-catenin and MUC1-C in nucleus. Simultaneously knockdown of GALNT6 and β-catenin significantly reduced the level of C-myc. Co-IP experiments indicated that GALNT6 interacted with MUC1-N, β-catenin interacting with MUC1-C in breast cancer cells. Together, our study reveals that GALNT6 promotes tumorigenicity and metastasis through β-catenin/MUC1-C signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 3C. * Yellow boxes: The mock and shRNA-NC panels appear to show an overlap ![file] , 
 #1 Dear Dr. Elisabeth M Bik, Thank you for pointing the error! We have revisited all the raw data of these experiments. Although we have all the original data and they fully support the conclusions of the paper, we regret the mistake, which accidentally used the data from the Mock group to represent the shRNA-NC group while omitting the actual data of the shRNA-NC group when we processed and assembled the data for this figure (Figure 3C). The raw data are attached below. We sincerely apologize for this unintentional error made before manuscript submission bur we failed to catch at the submission and subsequent review and publication steps. We are contacting the journal to correct the error. ![file] , 
 Correction, 11 November 2021: https: www.ijbs.com v17p4517.htm  *In our paper [1], the image of invaded MDA-MB-231 cells with empty vector transfection (shRNA-NC) in Figure 3C was mis-pasted. The image of invaded MDA-MB-231 cells (Mock) was accidentally used for u201cshRNA-NCu201d in Figure 3C. Neither the interpretation nor the conclusion of this work is affected by this error. Figure 3C should be corrected as follows.* I thank the authors for correcting this duplicated panel. ,