ArticleThe Journal of clinical investigation2010
Loss of Rab25 promotes the development of intestinal neoplasia in mice and is associated with human colorectal adenocarcinomas.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
91 citing papers in PubMed, 143 citations in OpenAlex.
- RAB25 modulates pit cell commitment by coordinating transforming growth factor-alpha secretion from gastric epithelial cells.Cell death & disease · 2025Article
- A proximity map of RAB GTPases delineates roles for RAB14 in EARP complex and UHRF1BP1 endosomal recruitments.Communications biology · 2025Article
- Function and regulation of Rab GTPases in cancers.Cell biology and toxicology · 2024Review
- The Role of Rab GTPases in the development of genetic and malignant diseases.Molecular and cellular biochemistry · 2024Review
- Rab25 suppresses colon cancer cell invasion through upregulating claudin‑7 expression.Oncology reports · 2024Article
- Molecular mechanisms of polarized transport to the apical plasma membrane.Frontiers in cell and developmental biology · 2024Review
- Tight Junction Claudins and Occludin Are Differentially Regulated and Expressed in Genomically Defined Subsets of Colon Cancer.Current issues in molecular biology · 2023Article
- Methylation-related genes involved in renal carcinoma progression.Frontiers in genetics · 2023Article
- Myosin Vb as a tumor suppressor gene in intestinal cancer.Oncogene · 2022Article
- iPSCs derived from esophageal atresia patients reveal SOX2 dysregulation at the anterior foregut stage.Disease models & mechanisms · 2022Article
- Recent advances in conventional and unconventional vesicular secretion pathways in the tumor microenvironment.Journal of biomedical science · 2022Review
- Targeted disruption of Rab1a causes early embryonic lethality.International journal of molecular medicine · 2022Article
- A SMAD4-modulated gene profile predicts disease-free survival in stage II and III colorectal cancer.Cancer reports (Hoboken, N.J.) · 2022Article
- Article
- Heritability and De Novo Mutations in Oesophageal Atresia and Tracheoesophageal Fistula Aetiology.Genes · 2021Review
- Developmental basis of trachea-esophageal birth defects.Developmental biology · 2021Review
- Article
- Rab25 acts as an oncogene and participates in the regulation of aerobic glycolysis via PKM2 in gastric adenocarcinoma.Translational cancer research · 2021Article
- Review
- Rab GTPases: Central Coordinators of Membrane Trafficking in Cancer.Frontiers in cell and developmental biology · 2021Review
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 2 countries.
Funding
Abstract
Transformation of epithelial cells is associated with loss of cell polarity, which includes alterations in cell morphology as well as changes in the complement of plasma membrane proteins. Rab proteins regulate polarized trafficking to the cell membrane and therefore represent potential regulators of this neoplastic transition. Here we have demonstrated a tumor suppressor function for Rab25 in intestinal neoplasia in both mice and humans. Human colorectal adenocarcinomas exhibited reductions in Rab25 expression independent of stage, with lower Rab25 expression levels correlating with substantially shorter patient survival. In wild-type mice, Rab25 was strongly expressed in cells luminal to the proliferating cells of intestinal crypts. While Rab25-deficient mice did not exhibit gross pathology, ApcMin/+ mice crossed onto a Rab25-deficient background showed a 4-fold increase in intestinal polyps and a 2-fold increase in colonic tumors compared with parental ApcMin/+ mice. Rab25-deficient mice had decreased beta1 integrin staining in the lateral membranes of villus cells, and this pattern was accentuated in Rab25-deficient mice crossed onto the ApcMin/+ background. Additionally, Smad3+/- mice crossed onto a Rab25-deficient background demonstrated a marked increase in colonic tumor formation. Taken together, these results suggest that Rab25 may function as a tumor suppressor in intestinal epithelial cells through regulation of protein trafficking to the cell surface.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.