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MicroRNA expression profile between KRAS/BRAF wild and BRAF mutant colorectal cancer

ABSTRACT: The genome-wide miRNA expression analysis was performed in clinical samples, comprising 15 BRAF-mutant and 15 non-KRAS/BRAF-mutant colorectal cancers by using a SurePrint G3 Human miRNA microarray.

ORGANISM(S): Homo sapiens

PROVIDER: GSE66548 | GEO | 2016/04/01

SECONDARY ACCESSION(S): PRJNA277301

REPOSITORIES: GEO

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microRNA expression profile between KRAS/BRAF wild and BRAF mutant colorectal cancer

Project description:The genome-wide miRNA expression analysis was performed in clinical samples, comprising 15 BRAF-mutant and 15 non-KRAS/BRAF-mutant colorectal cancers by using a SurePrint G3 Human miRNA microarray. clinical samples, comprising 15 BRAF-mutant and 15 non-KRAS/BRAF-mutant colorectal cancers by using a SurePrint G3 Human miRNA microarray.

2016-04-01 | E-GEOD-66548 | biostudies-arrayexpress

Mutant KRAS/BRAF Reprograms the Enhancer Landscape via GATA1 to Drive Chemoresistance

Project description:Despite advances in the detection and management of colorectal cancers, resistance to anti-cancer therapies remains a significant challenge. Activating mutations in KRAS and BRAF are frequently observed in colorectal cancers and have been associated with aggressive tumors and poor survival after chemotherapy. In the present study, we demonstrate that mutations in KRAS/BRAF alter the enhancer landscape of tumor cells, which leads to the resistance of the cornerstone colorectal cancer chemotherapeutic agent 5-fluorouracil (5-FU) through activation of transcription factor GATA1. Targeted inhibition of GATA1 reverses epigenetic changes in KRAS mutant cells and restores sensitivity to 5-FU. These results indicate a novel therapeutic opportunity for tailoring individualized therapy in human colorectal cancer.

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Oncogenic KRAS(G12V) and BRAF(V600E) in intestinal organoids

Project description:Goals of the study was to compare transcripional and phenotypic response of mouse intestinal organoid cultures to the KRAS(G12V) or BRAF(V600E)oncogenes.

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Oncogenic KRAS and BRAF drive metabolic reprogramming in colorectal cancer JEH 2016

Project description:Multiplexed PRM analysis for metabolic reprogramming in isogenic cell lines with KRAS or BRAF mutations.

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BRAF-induced tumorigenesis is IKKalpha dependent but NF?B independent

Project description:Tumor cells carrying KRAS mutations activate the NF-?B pathway by different mechanisms, which contribute to the acquisition of essential cancer properties. The BRAF kinase, a downstream mediator of KRAS, is also mutated in a subset of colorectal cancers (CRC), which predicts bad prognosis and therapy resistance. However, nothing is known on whether NF-?B participates of BRAF-mediated tumorigenesis. We here found that in CRC cells, mutant BRAF does not trigger canonical or alternative NF-?B signaling but induces p45-IKK? activation. Moreover, IKK? activity is required for BRAF-induced transformation and to support BRAF-dependent transcription in CRC cells. Activation of p45-IKK? downstream of BRAF requires the TAK1 kinase, and is associated to the endosomal compartment. Inhibition of endosomal V-ATPase abolished p45-IKK? phosphorylation, and induced apoptosis of BRAF mutated CRC cells. Pharmacologic inhibition of endosome acidification reduced the in vivo growth of tumors carrying mutant BRAF, and abrogated the metastatic capacity of a primary human CRC tumor with acquired resistance to standard chemotherapy in an orthotopic xenograft model. 18 samples were analyzed: HT29 controls (n=3); HT28 BRAF inhibited (n=3), WiDr controls (n=3); WiDr BRAF inhibited (n=3); WiDr transduced with control shRNA (n=3) and WiDr transduced with shRNA against IKKalpha (n=3)

2015-05-08 | E-GEOD-57979 | biostudies-arrayexpress

BRAF-induced tumorigenesis is IKKalpha dependent but NFκB independent

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Project description:Murine skin tumors following combintions of Braf, Alk5, p53, Tgfbr2 and Kras mutation, under the control of Lgr5CreER.

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Mutant KRAS/BRAF Reprograms the Enhancer Landscape via GATA1 to Drive Chemoresistance

Project description:Mutant KRAS/BRAF Reprograms the Enhancer Landscape via GATA1 to Drive Chemoresistance

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The RALA pathway can maintain the proliferation of KRAS- and BRAF-mutated cancer cells

Project description:By silencing of RALA, a downstream member of the RAS signal transduction pathway, we aimed to determine whether genes downstream of a mutated KRAS (codon 12 or 13) or a mutated BRAF can have significant functions in colorectal cancer carcinogenesis.

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Project description:Oncogenic KRAS(G12V) and BRAF(V600E) in intestinal organoids

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