ArticleNeoplasia (New York, N.Y.)2009
BRAF(V600E) efficient transformation and induction of microsatellite instability versus KRAS(G12V) induction of senescence markers in human colon cancer cells.
Article in Neoplasia (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
27 citing papers in PubMed, 44 citations in OpenAlex.
- AI-driven virtual cell models in preclinical research: technical pathways, validation mechanisms, and clinical translation potential.NPJ digital medicine · 2025Review
- Oncogene-Induced Senescence Transcriptomes Signify Premalignant Colorectal Adenomas.Current issues in molecular biology · 2025Article
- KRAS Mutation Subtypes and Their Association with Other Driver Mutations in Oncogenic Pathways.Cells · 2024Review
- Synergistic eradicating impact of 5-fluouracil with FeO nanoparticles-diethyldithiocarbamate in colon cancer spheroids.Nanomedicine (London, England) · 2024Article
- Article
- Selective Activation of MCancers · 2023Article
- [Detection of BRAF V600E mutation in metastatic colorectal carcinoma : A QuIP round robin test].Der Pathologe · 2022Review
- The Real-Life Data of BRAF Mutation on the Treatment of Colorectal Cancer: a TOG Study.Journal of gastrointestinal cancer · 2021Article
- Molecular targeted therapy ofTherapeutic advances in medical oncology · 2019Review
- Association of BRAF Mutations With Survival and Recurrence in Surgically Treated Patients With Metastatic Colorectal Liver Cancer.JAMA surgery · 2018Article
- Liver fluke infection and cholangiocarcinoma: a review.Parasitology research · 2017Review
- Important molecular genetic markers of colorectal cancer.Oncotarget · 2016Review
- Article
- Increased Expression of Serglycin in Specific Carcinomas and Aggressive Cancer Cell Lines.BioMed research international · 2015Article
- Preparation and characterization of anti-HIV nanodrug targeted to microfold cell of gut-associated lymphoid tissue.International journal of nanomedicine · 2015Article
- BRAF vs RAS oncogenes: are mutations of the same pathway equal? Differential signalling and therapeutic implications.Oncotarget · 2014Review
- The role of cellular senescence in the gastrointestinal mucosa.Gut and liver · 2013Article
- Distinct requirement for an intact dimer interface in wild-type, V600E and kinase-dead B-Raf signalling.The EMBO journal · 2012Article
- CpG Island Methylation, Microsatellite Instability, and BRAF Mutations and Their Clinical Application in the Treatment of Colon Cancer.Chemotherapy research and practice · 2012Article
- The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In colorectal cancer, BRAF and KRAS oncogenes are mutated in about 15% and 35% respectively at approximately the same stage of the adenoma-carcinoma sequence. Since these two mutations rarely coexist, further analysis to dissect their function of transformation in colon cancer is required. Caco-2 human colon adenocarcinoma cells were stably transfected with BRAF(V600E) (Caco-BR cells) or KRAS(G12V) (Caco-K cells) oncogenes. BRAF(V600E) is more efficient in transforming Caco-2 cells and altering their morphology. The dominant nature of BRAF(V600E) is evident by its ability to render Caco-2 cells tumorigenic in vivo all be it through selective extracellular signal-related kinase (ERK) 2 phosphorylation and high levels of cyclin D1. As a consequence, the cell cycle distribution of parental cells is altered and microsatellite instability is introduced. Attenuated ERK activation observed correlated with KSR downregulation by BRAF(V600E) without further implications to signaling. Highly activated ERK in case of KRAS(G12V) (Caco-K cells) leads to mild transformation causing Caco-K cells to express premature senescence-related markers and acquire growth factor-dependent viability. Interestingly, BRAF(WT)gets equally activated by upstream KRAS mutations present in colon adenocarcinoma cells such as DLD-1 and SW620. Taken together, these results suggest that the two oncogenes have different transforming capability in colon cancer, although they both use the mitogen-activated protein (MAP) kinase pathway to carry out their effect. In general, BRAF(V600E) presents greater potential in mediating tumorigenic effect as compared to KRAS(G12V) both in vivo and in vitro. These findings may have implications in personalised diagnosis and targeted therapeutics.
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