ArticleMolecular cancer2010
Krüppel-like factor 5 is a crucial mediator of intestinal tumorigenesis in mice harboring combined ApcMin and KRASV12 mutations.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- KLF family of proteins in gastrointestinal tumors (Review).Oncology letters · 2026Review
- New insights into KLFs and SOXs in cancer pathogenesis, stemness, and therapy.Seminars in cancer biology · 2023Review
- Review
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
- Krüppel-like factor 5 is upregulated and induces cell proliferation in endometrial cancer.Oncology letters · 2021Article
- KLF5 Is Activated by Gene Amplification in Gastric Cancer and Is Essential for Gastric Cell Proliferation.Cells · 2021Article
- miR-320-3p regulates the proliferation, migration and apoptosis of hypoxia-induced pulmonary arterial smooth muscle cells via KLF5 and HIF1α.American journal of translational research · 2021Article
- F-Box Proteins and Cancer.Cancers · 2020Review
- microRNA-195 attenuates neuronal apoptosis in rats with ischemic stroke through inhibiting KLF5-mediated activation of the JNK signaling pathway.Molecular medicine (Cambridge, Mass.) · 2020Article
- The Novel Small-Molecule SR18662 Efficiently Inhibits the Growth of Colorectal CancerMolecular cancer therapeutics · 2019Article
- Genetic Aberration Analysis in Thai Colorectal Adenoma and Early-Stage Adenocarcinoma Patients by Whole-Exome Sequencing.Cancers · 2019Article
- CINP is a novel cofactor of KLF5 required for its role in the promotion of cell proliferation, survival and tumor growth.International journal of cancer · 2019Article
- KLF5 mediates the hyper-proliferative phenotype of the intestinal epithelium in mice with intestine-specific endogenous K-RasAmerican journal of cancer research · 2018Article
- SP and KLF Transcription Factors in Digestive Physiology and Diseases.Gastroenterology · 2017Review
- Krüppel-like factors in mammalian stem cells and development.Development (Cambridge, England) · 2017Review
- Aging and the Krüppel-like factors.Trends in cell & molecular biology · 2017Article
- Improved Swiss-rolling Technique for Intestinal Tissue Preparation for Immunohistochemical and Immunofluorescent Analyses.Journal of visualized experiments : JoVE · 2016Article
- ML264, A Novel Small-Molecule Compound That Potently Inhibits Growth of Colorectal Cancer.Molecular cancer therapeutics · 2016Article
- Role of Krüppel-like factors in cancer stem cells.Journal of physiology and biochemistry · 2015Review
- Interruption of KLF5 acetylation converts its function from tumor suppressor to tumor promoter in prostate cancer cells.International journal of cancer · 2015Article
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6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundBoth mutational inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene and activation of the KRAS oncogene are implicated in the pathogenesis of colorectal cancer. Mice harboring a germline ApcMin mutation or intestine-specific expression of the KRASV12 gene have been developed. Both mouse strains develop spontaneous intestinal tumors, including adenoma and carcinoma, though at a different age. The zinc finger transcription factor Krüppel-like factor 5 (KLF5) has previously been shown to promote proliferation of intestinal epithelial cells and modulate intestinal tumorigenesis. Here we investigated the in vivo effect of Klf5 heterozygosity on the propensity of ApcMin/KRASV12 double transgenic mice to develop intestinal tumors.
resultsAt 12 weeks of age, ApcMin/KRASV12 mice had three times as many intestinal tumors as ApcMin mice. This increase in tumor number was reduced by 92% in triple transgenic ApcMin/KRASV12/Klf5+/- mice. The reduction in tumor number in ApcMin/KRASV12/Klf5+/- mice was also statistically significant compared to ApcMin mice alone, with a 75% decrease. Compared with ApcMin/KRASV12, tumors from both ApcMin/KRASV12/Klf5+/- and ApcMin mice were smaller. In addition, tumors from ApcMin mice were more distally distributed in the intestine as contrasted by the more proximal distribution in ApcMin/KRASV12 and ApcMin/KRASV12/Klf5+/- mice. Klf5 levels in the normal-appearing intestinal mucosa were higher in both ApcMin and ApcMin/KRASV12 mice but were attenuated in ApcMin/KRASV12/Klf5+/- mice. The levels of beta-catenin, cyclin D1 and Ki-67 were also reduced in the normal-appearing intestinal mucosa of ApcMin/KRASV12/Klf5+/- mice when compared to ApcMin/KRASV12 mice. Levels of pMek and pErk1/2 were elevated in the normal-appearing mucosa of ApcMin/KRASV12 mice and modestly reduced in ApcMin/KRASV12/Klf5+/- mice. Tumor tissues displayed higher levels of both Klf5 and beta-catenin, irrespective of the mouse genotype from which tumors were derived.
conclusionsResults of the current study confirm the cumulative effect of Apc loss and oncogenic KRAS activation on intestinal tumorigenesis. The drastic reduction in tumor number and size due to Klf5 heterozygosity in ApcMin/KRASV12 mice indicate a critical function of KLF5 in modulating intestinal tumor initiation and progression.
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