PGM3 regulates beta-catenin activity to promote colorectal cancer cell progression

Author:

Zhang Nan1ORCID,Liu Si1,Xu Junxuan1,Ning Tingting1,Xie Sian1,Min Li1,Zhu Shengquan1,Zhang Shutian1,Zhu Shengtao1

Affiliation:

1. Department of Gastroenterology, Beijing Friendship Hospital, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, Capital Medical University, Beijing 100050, P.R. China

Abstract

The hexosamine biosynthetic pathway (HBP) is connected to abnormal N- and O-linked protein glycosylation in cancer, which performs critical roles in tumorigenesis. However, the regulation mechanisms of HBP and its role in colorectal cancer (CRC) progression remain unexplained. This study analyzed the expression level of phosphoglucomutase 3 (PGM3), a key enzyme in HBP, and identified its function in CRC cell lines. Analysis of publicly available CRC microarray data determined that PGM3 is upregulated in CRC tumor tissues. Furthermore, functional experiments emphasized the significant roles of PGM3 in facilitating CRC cell proliferation and migration. Mechanistically, we demonstrated that the activity of β-catenin in CRC was maintained by PGM3-mediated O-GlcNAcylation. PGM3 knockdown or inhibition of O-GlcNAc transferase decreased β-catenin activity and the expression levels of its downstream targets. Collectively, our findings indicate that PGM3 exhibits tumor-promoting roles by elevating O-GlcNAcylation level and maintaining β-catenin activity, and might serve as a prognostic biomarker and treatment target in CRC.

Funder

Research Foundation of Beijing Friendship Hospital, Capital Medical University

National Natural Science Foundation of China

Publisher

SAGE Publications

Subject

General Biochemistry, Genetics and Molecular Biology

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