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The PP2A regulator IER5L supports prostate cancer progression

ABSTRACT: The PP2A regulator IER5L supports prostate cancer progression

PROVIDER: PRJNA1048860 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27076289_1.fastq.gz	Fastqsanger.gz
	SRR27076289_2.fastq.gz	Fastqsanger.gz
	SRR27076290_1.fastq.gz	Fastqsanger.gz
	SRR27076290_2.fastq.gz	Fastqsanger.gz
	SRR27076291_1.fastq.gz	Fastqsanger.gz

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The PP2A regulator IER5L supports prostate cancer progression

Project description:Prostate cancer exhibits high prevalence and accounts for a high number of cancer-related deaths. The discovery and characterization of molecular determinants of aggressive prostate cancer represents an active area of research. The Immediate Early Response (IER) family of genes, which regulate Protein Phosphatase 2A (PP2A) activity, has emerged among the factors that influence cancer biology. Here, we show that the less studied member of this family, Immediate Early Response 5 like (IER5L), is upregulated in aggressive prostate cancer. Interestingly, the upregulation of IER5L expression exhibits a robust association with metastatic disease in prostate and is recapitulated in other cancer types. In line with this observation, IER5L silencing reduces foci formation, migration and invasion ability in a variety of human and murine prostate cancer cell lines. In vivo, using zebrafish and immunocompromised mice models, we demonstrate that IER5L is required for prostate cancer tumor growth, dissemination, and metastasis. Mechanistically, we characterize the transcriptomic and proteomic landscapes of IER5L-silenced cells. This approach allowed us to identify DNA replication and monomeric G protein regulators as downstream programs of IER5L through a pathway that is consistent with the regulation of PP2A. In sum, we report the alteration of IER5L in prostate cancer and beyond and provide biological and molecular evidence of its contribution to tumor aggressiveness.

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A metabolic co-regulator bioinformatics screen reveals that PGC1Î± suppresses prostate cancer metastasis

Project description:The current view of cellular transformation and cancer progression supports the notion that cancer cells must reprogram their metabolism in order to survive and progress in different microenvironments. Master co-regulators of metabolism orchestrate the modulation of multiple metabolic pathways through transcriptional programs, and hence constitute a probabilistically parsimonious mechanism for general metabolic rewiring. Here we show that the transcriptional co-activator PGC1Î± suppresses prostate cancer progression and metastasis. A metabolic co-regulator data mining analysis unveiled that PGC1Î± is consistently down-regulated in multiple prostate cancer patient datasets and its alteration is associated with reduced disease-free survival and metastasis. Genetically engineered mouse model studies revealed that compound prostate epithelium-specific deletion of Pgc1a and Pten promotes prostate cancer progression and metastasis, whereas, conversely, PGC1Î± expression in cell lines inhibits the pre-existing metastatic capacity. Through the application of integrative metabolomics and transcriptomics we demonstrate that PGC1Î± expression in prostate cancer is sufficient to elicit a global metabolic rewiring that opposes cell growth, consisting of sustained oxidative metabolism at the expense of anabolism. This metabolic program is regulated downstream the Oestrogen-related receptor alpha (ERRÎ±), and PGC1Î± mutants lacking ERRÎ± activation capacity lack metabolic rewiring capacity and metastasissuppressive function. Importantly, an ERRÎ± signature in prostate cancer recapitulates the prognostic features of PGC1A. Our findings uncover an unprecedented causal contribution of PGC1Î± to the metabolic switch in prostate cancer and to the suppression of metastatic dissemination. Total RNA was isolated from prostate cancer cell line PC3 expressing or not PGC1a (for induction, cells were treated with doxycycline for 2 passages)

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