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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE39857 | GEO | 2015/06/20

SECONDARY ACCESSION(S): PRJNA171925

REPOSITORIES: GEO

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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. RALA was silenced in three colorectal cancer cell lines (SW480, HCT116 and HT29). Effects were normalized to mock-transfected cells and the effects of scramble siRNA were excluded. SW480, HCT116 and HT29 cell lines were treated with the PI3K inhibitor LY294002 or DMSO.

2015-06-20 | E-GEOD-39857 | biostudies-arrayexpress

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

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

Project description:Tumor cells carrying KRAS mutations activate the NF-κB 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-κB participates of BRAF-mediated tumorigenesis. We here found that in CRC cells, mutant BRAF does not trigger canonical or alternative NF-κB signaling but induces p45-IKKα activation. Moreover, IKKα activity is required for BRAF-induced transformation and to support BRAF-dependent transcription in CRC cells. Activation of p45-IKKα downstream of BRAF requires the TAK1 kinase, and is associated to the endosomal compartment. Inhibition of endosomal V-ATPase abolished p45-IKKα 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.

2015-05-08 | GSE57979 | GEO

Targeted treatment for KRAS/BRAF-mutated and BCL2L1-amplified CRCs

Project description:A novel combination treatment targeting BCL2L1 and MCL1 for KRAS/BRAF-mutated and BCL2L1-amplified colorectal cancers

| PRJEB20153 | ENA

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

2016-04-01 | GSE66548 | GEO

GNPS - 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.

2016-02-01 | MSV000079486 | GNPS

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.

2018-06-02 | GSE115234 | GEO

Radiation combined with KRAS-MEK inhibitors enhances anticancer immunity in KRAS-mutated tumor models [LLC RNA-seq]

Project description:KRAS mutation is a common driver in solid tumors, and KRAS-mutated tumors are relatively resistant to radiotherapy. Therefore, we investigated the combined effect of radiation and KRAS-MEK inhibitors (AMG510 and trametinib) in KRAS-mutated tumors.

2022-10-01 | GSE209766 | GEO

Radiation combined with KRAS-MEK inhibitors enhances anticancer immunity in KRAS-mutated tumor models [CT26 RNA-seq]

2022-10-01 | GSE209765 | GEO

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