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An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2 [ChIP-Seq]

ABSTRACT: An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2 [ChIP-Seq]

PROVIDER: PRJNA541244 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9017080.fastq.gz	Fastqsanger.gz
	SRR9017090.fastq.gz	Fastqsanger.gz
	SRR9017081.fastq.gz	Fastqsanger.gz
	SRR9017091.fastq.gz	Fastqsanger.gz
	SRR9017082.fastq.gz	Fastqsanger.gz

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An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2 [array]

Project description:Perturbations in histone modifications alter transcription and promote carcinogenesis. Breast cancers frequently overexpress the histone methyltransferase EZH2, the catalytic subunit of Polycomb Repressor Complex 2 (PRC2). However, the mechanisms driving EZH2 overexpression are obscure and elucidating the role of PRC2 in breast cancer, which is highly heterogeneous, is challenging given its context-dependent oncogenic and tumor suppressive functions. Here, using genetically engineered mouse, PDX and cell line models, we show that the tyrosine kinase c-Src links energy sufficiency with PRC2 subunit overexpression via control of mRNA translation. In breast cancers initiated by the oncogene ErbB2, c-Src stimulates mitochondrial ATP production to suppress energy stress and permit sustained activation of the mammalian/mechanistic target of rapamycin complex 1 (mTORC1), which increases the translation of mRNAs encoding the PRC2 subunits Ezh2 and Suz12. We show that Ezh2 overexpression and activity are pivotal in ErbB2-mediated mammary tumorigenesis. These results reveal the hitherto unknown c-Src/mTORC1/PRC2 axis, which is essential for ErbB2-driven carcinogenesis.

2018-01-31 | GSE93892 | GEO

An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2 [RNA-Seq]

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An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2 [ChIP-Seq]

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An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2

Project description:An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2

| PRJNA541243 | ENA

An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2 [RNA-Seq]

Project description:An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2 [RNA-Seq]

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An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2

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

2019-05-06 | GSE130739 | GEO

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Project description:An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2 [array]

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Individual SRC-2 and SRC-3 knock-down in MCF-7 cells

Project description:Experimental aim: identification of SRC-2 and SRC-3-related genes in MCF-7 breast cancer cells. Experimental workflow: 1. shRNA transduction. MCF-7 cells were transduced with a mix of lentiviral particles containing five individual lentiviral pLKO.1-puro short hairpin (sh) RNA plasmids targeting different sequences on SRC-2 or SRC-3 mRNA and a pLKO.1-puro empty vector control. The puromycin selections were maintained for three weeks to obtain cells containing stably integrated shRNA. 2. Sample preparation. RNA was extracted from eight independent replicates expressing the pLKO.1-puro empty shRNA vector (shKTR), from eight replicates of SRC-2 shRNA expressing cells (shSRC-2), and from seven replicates of SRC-3 shRNA expressing cells (shSRC-3). 300 ng of total RNA from each cell sample was biotin-labelled and amplified.

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Microarray analysis of ErbB2-driven mouse mammary tumour cells treated with GSK-126

Project description:Monoclonal antibodies (mAbs) targeting the oncogenic receptor tyrosine kinase ERBB2/HER2, such as Trastuzumab, are the standard of care therapy for breast cancers driven by ERBB2 overexpression and activation. However, a substantial proportion of patients exhibits de novo resistance. Here, by comparing matched Trastuzumab-naïve and post-treatment patient samples from a neoadjuvant trial, we link resistance with elevation of H3K27me3, a repressive histone modification catalyzed by Polycomb Repressor Complex 2 (PRC2). In ErbB2+ breast cancer models, PRC2 silences endogenous retroviruses (ERVs) to suppress anti-tumor Type-I interferon (IFN) responses. In patients, elevated H3K27me3 in tumor cells following Trastuzumab treatment correlates with suppression of IFN-driven viral defense gene expression signatures and poor response. Using an immunocompetent model, we provide evidence that EZH2 inhibitors promote IFN-driven immune responses that enhance the efficacy of anti-ErbB2 mAbs, suggesting the potential clinical benefit of epigenomic reprogramming by H3K27me3 depletion in Trastuzumab-resistant disease.

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