GOLM1 restricts colitis and colon tumorigenesis by ensuring Notch signaling equilibrium in intestinal homeostasis
Open accessAbstract
Intestinal epithelium serves as the first barrier against the infections and injuries that mediate colonic inflammation. Colorectal cancer is often accompanied with chronic inflammation. Differed from its well-known oncogenic role in many malignancies, we present here that Golgi membrane protein 1 (GOLM1, also referred to as GP73) suppresses colorectal tumorigenesis via maintenance of intestinal epithelial barrier. GOLM1 deficiency in mice conferred susceptibility to mucosal inflammation and colitis-induced epithelial damage, which consequently promoted colon cancer. Mechanistically, depletion of GOLM1 in intestinal epithelial cells (IECs) led to aberrant Notch activation that interfered with IEC differentiation, maturation, and lineage commitment in mice. Pharmacological inhibition of Notch pathway alleviated epithelial lesions and restrained pro-tumorigenic inflammation in GOLM1-deficient mice. Therefore, GOLM1 maintains IEC homeostasis and protects against colitis and colon tumorigenesis by modulating the equilibrium of Notch signaling pathway.
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Dysregulation of GARGs has been implicated in tumor progression, therapy resistance, and remodeling of the immune microenvironment across multiple cancer types.
“Dysregulation of GARGs has been implicated in tumor progression, therapy resistance, and remodeling of the immune microenvironment across multiple cancer types.”
From Construction and validation of golgi apparatus-related genes as predictors of the immune microenvironment and prognosis in colorectal cancer (2026) · cites this paper as [15]
The Introduction (page unavailable) links GOLM1 to oncogenic activity in multiple cancers and to immunoregulation, including macrophage polarization. The Discussion (page unavailable) describes its cancer role as tissue- and context-dependent. The paper does not establish the broader claim about GARGs as a group, therapy resistance, or remodeling of the immune tumor microenvironment across cancer types. (LLM, conf=0.86)
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References 49 · Cited by 50
- Authors
- Pu, Y., Song, Y., Zhang, M., Long, C., Li, J., Wang, Y., Xu, Y., Pan, F., Zhao, N., Zhang, X., Xu, Y., Cui, J., Wang, H., Li, Y., Zhao, Y., Jin, D., & Zhang, H.
- Affiliations
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Dalian Medical University (CN)
- Chinese Academy of Sciences (CN)
- Chinese PLA General Hospital (CN)
- Shanghai Jiao Tong University (CN)
- Corresponding author
- Pu, Yang
- Jin, Di
- Zhang, Hongbing
- ORCID
- Venue
- Signal Transduction and Targeted Therapy
- Published
- 2021-04-14
- Volume
- 6
- Issue
- 1
- Pages
- 148-148
- ISSN
- 2059-3635 (ISSN-L)
- PMC
- PMC8044123
- OpenAlex
- W3152816756
- Cited by
- 50
- References
- 49
- Citations by year
- 2026: 7 · 2025: 16 · 2024: 9 · 2023: 7 · 2022: 8 · 2021: 3
- FWCI
- 3.82
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Signal Transduction and Targeted Therapy (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81730078, 31700785, 81602456, 81800552)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- GOLM1, GP73, Notch signaling, colitis, colon tumorigenesis, colorectal cancer, intestinal epithelial barrier, intestinal homeostasis, intestinal epithelial cells, epithelial differentiation, inflammation-associated cancer
- MeSH terms
- Animals, Colitis, Colon, Colonic Neoplasms, Epithelial Cells, Humans, Intestines, Membrane Proteins, Phosphoproteins, Signal Transduction, Mice, Receptors, Notch
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