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MYC-driven small-cell lung cancer is metabolically distinct and vulnerable to arginine depletion

ABSTRACT: MYC-driven small-cell lung cancer is metabolically distinct and vulnerable to arginine depletion

PROVIDER: PRJNA597163 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10753547.fastq.gz	Fastqsanger.gz
	SRR10753549.fastq.gz	Fastqsanger.gz
	SRR10753550.fastq.gz	Fastqsanger.gz
	SRR10753551.fastq.gz	Fastqsanger.gz
	SRR10753552.fastq.gz	Fastqsanger.gz

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MYC-driven small-cell lung cancer is metabolically distinct and vulnerable to arginine depletion

Project description:We report ChIP-Seq analyses for MYC and H3K27Ac in tumors from our MYC-driven genetically engineered mouse model of small cell lung cancer (SCLC) infected with Ad-Cgrp-Cre

2019-12-22 | GSE142496 | GEO

MYC-Driven Small-Cell Lung Cancer is Metabolically Distinct and Vulnerable to Arginine Depletion.

Project description:PurposeSmall-cell lung cancer (SCLC) has been treated clinically as a homogeneous disease, but recent discoveries suggest that SCLC is heterogeneous. Whether metabolic differences exist among SCLC subtypes is largely unexplored. In this study, we aimed to determine whether metabolic vulnerabilities exist between SCLC subtypes that can be therapeutically exploited.Experimental designWe performed steady state metabolomics on tumors isolated from distinct genetically engineered mouse models (GEMM) representing the MYC- and MYCL-driven subtypes of SCLC. Using genetic and pharmacologic approaches, we validated our findings in chemo-naïve and -resistant human SCLC cell lines, multiple GEMMs, four human cell line xenografts, and four newly derived PDX models.ResultsWe discover that SCLC subtypes driven by different MYC family members have distinct metabolic profiles. MYC-driven SCLC preferentially depends on arginine-regulated pathways including polyamine biosynthesis and mTOR pathway activation. Chemo-resistant SCLC cells exhibit increased MYC expression and similar metabolic liabilities as chemo-naïve MYC-driven cells. Arginine depletion with pegylated arginine deiminase (ADI-PEG 20) dramatically suppresses tumor growth and promotes survival of mice specifically with MYC-driven tumors, including in GEMMs, human cell line xenografts, and a patient-derived xenograft from a relapsed patient. Finally, ADI-PEG 20 is significantly more effective than the standard-of-care chemotherapy.ConclusionsThese data identify metabolic heterogeneity within SCLC and suggest arginine deprivation as a subtype-specific therapeutic vulnerability for MYC-driven SCLC.

| S-EPMC6697617 | biostudies-literature

Metabolic engineering of Corynebacterium glutamicum for L-arginine production

Project description:Metabolically engineered Corynebacterium glutamicum strains were constructed for the enhanced production of L-arginine, and their gene expression profiles were investigated Gene expression profiles of two C. glutamicum strains AR2 and AR6 were examined for the 3043 genes twice.

2013-11-26 | E-GEOD-52737 | biostudies-arrayexpress

Metabolic engineering of Corynebacterium glutamicum for L-arginine production

Project description:Metabolically engineered Corynebacterium glutamicum strains were constructed for the enhanced production of L-arginine, and their gene expression profiles were investigated

2013-11-26 | GSE52737 | GEO

EZH2 depletion potentiates MYC degradation inhibiting neuroblastoma and small cell carcinoma tumor formation

Project description:Efforts to therapeutically target EZH2 have generally focused on inhibition of its methyltransferase activity, although it remains less clear whether this is the central mechanism whereby EZH2 promotes cancer. We demonstrate that EZH2 directly interacts with both MYC family oncoproteins, MYC and MYCN, and promotes their stabilization in a methyltransferase-independent manner. By competing against the SCFFBW7 ubiquitin ligase to bind MYC and MYCN, EZH2 counteracted FBW7-mediated MYC(N) polyubiquitination and proteasomal degradation. Depletion, but not enzymatic inhibition, of EZH2 induced robust MYC(N) degradation and inhibited tumor cell growth in MYC(N) driven neuroblastoma and small cell lung cancer. These findings unveil the MYC family proteins as global EZH2 oncogenic effectors and EZH2 pharmacologic degraders as potential MYC(N) targeted cancer therapeutics, pointing out that MYC(N) driven cancers may develop inherent resistance to the canonical EZH2 enzymatic inhibitors currently in clinical development.

2022-02-17 | PXD029652 | Pride

Lung macrophages mediate helminth resistance through differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion

Project description:Lung macrophages mediate helminth resistance through differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion

2022-01-13 | GSE189674 | GEO

Systems level profiling of arginine starvation in ASS1 negative sarcomas reveals ERK and MYC adaptive metabolic reprogramming of TCA anaplerosis and lipid metabolism

Project description:submission for the paper "Systems level profiling of arginine starvation in ASS1 negative sarcomas reveals ERK and MYC adaptive metabolic reprogramming of TCA anaplerosis and lipid metabolism"

2020-01-09 | MSV000084785 | MassIVE

Transcription profiling of human carcinoma LS174T cells following depletion of Myc and Usp28 using shRNA

Project description:Analysis of gene expression following depletion of Myc and Usp28 using shRNA in colon carcinoma LS174T cells.

2007-04-19 | E-MEXP-1070 | biostudies-arrayexpress

RNA-SEQ analysis of KMC murine pancreatic ductal adenocarcinoma (PDAC) cell line upon siRNA depletion of MYC, KRas or Miz1 (aka Zbtb17)

Project description:MYC is varyingly thought to either complement KRAS or to act as a downstream KRAS effector - here we compared the transcriptomic impact of MYC depletion with that of KRas depletion in a cell line derived from PDAC driven by lsl-KRas^G12D + Rosa26-lsl-MYC^DM. A second question addressed related to the mechanism of MYC-dependent transcriptional repression, which in many instances requires MYC binding to Miz1. We therefore included analysis of Miz1-depleted KMC cells in this experiment

2020-03-16 | E-MTAB-8792 | biostudies-arrayexpress

Transcriptional profiling of MDA-MB-231 and its ρ0 cells (lacking mtDNA) after 48h arginine depletion by arginine deiminase (ADI).

Project description:Transcriptional profiling of MDA-MB-231 and its ρ0 cells (lacking mtDNA) after 48h arginine depletion by arginine deiminase (ADI).

| PRJNA408268 | ENA

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