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A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers

ABSTRACT: A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers

PROVIDER: PRJNA487264 | ENA |

REPOSITORIES: ENA

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A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers [inhibitors]

Project description:A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers [inhibitors]

| PRJNA487269 | ENA

A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers [HOXC10]

Project description:A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers [HOXC10]

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A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers [inhibitors]

Project description:MEK and BRD4 inhibitors induce cell death of subset of KRAS-mutant lung tumors in vitro and in vivo We performed microarray analysis of MEK and BRD4 inhibition alone and in combination 24 hours after treatment, prior to the induction of cell death, to analyze transcriptional changes that might be mechanistic drivers of the therapeutic effect

2020-04-02 | GSE118903 | GEO

A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-04-02 | GSE118909 | GEO

A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers [HOXC10]

Project description:HOXC10 overexpression modifies the therapeutic response to combined MEK and BRD4 inhibitors We performed microarray analysis of cells expressing LACZ or HOXC10 treated with MEK and BRD4 inhibition in combination for 24 hours, prior to the induction of cell death, to analyze transcriptional changes that might be mechanistic drivers of the therapeutic effect.

2020-04-02 | GSE118908 | GEO

Oncogenic KRAS induces arginine auxotrophy in non-small cell lung cancer and confers a therapeutic vulnerability to SLC7A1 inhibition

Project description:The urea cycle is frequently rewired in cancer cells to meet the metabolic demands of cancer, yet our understanding about the regulatory mechanisms for this pathway in different types of cancer is very limited. In this study, we discover that oncogenic activation of KRAS in non-small cell lung cancer (NSCLC) silences the expression of arginosuccinate synthase 1 (ASS1), a urea cycle enzyme catalyzing the production of arginine from aspartate and citrulline, and thereby diverts the utilization of aspartate to pyrimidine synthesis to meet the high demand for DNA replication in KRAS-mutant NSCLC. Specifically, KRAS signaling facilitates a hypo-acetylated state in the promoter region of ASS1 gene in a histone deacetylase 3 (HDAC3)-dependent manner, which in turn impedes the recruitment of the transcription factor c-MYC for ASS1 transcription. ASS1 suppression in KRAS-mutant NSCLC cancer cells impairs the biosynthesis of arginine and renders growth dependency on SLC7A1, an arginine transmembrane transport, to import extracellular arginine. Depletion of SLC7A1 in both patient-derived organoid and xenograft models obtains a substantial therapeutic benefit in inhibiting KRAS-driven NSCLC growth. Together, our findings uncover a new role of oncogenic KRAS in rewiring urea cycle metabolism and identify SLC7A1-mediated arginine uptake as a therapeutic vulnerability in treating KRAS-mutant NSCLC.

2024-01-20 | GSE253688 | GEO

Oncogenic KRAS induces arginine auxotrophy in non-small cell lung cancer and confers a therapeutic vulnerability to SLC7A1 inhibition

Project description:Oncogenic KRAS induces arginine auxotrophy in non-small cell lung cancer and confers a therapeutic vulnerability to SLC7A1 inhibition

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Project description:BCL6 confers KRAS-mutant NSCLCs resistance to BET inhibitors [ChIP-Seq]

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