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TIP5 primes prostate luminal cells for the oncogenic transformation mediated by PTEN-loss

ABSTRACT: TIP5 primes prostate luminal cells for the oncogenic transformation mediated by PTEN-loss

PROVIDER: PRJNA545111 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9136320.fastq.gz	Fastqsanger.gz
	SRR9136330_1.fastq.gz	Fastqsanger.gz
	SRR9136330_2.fastq.gz	Fastqsanger.gz
	SRR9136321.fastq.gz	Fastqsanger.gz
	SRR9136331_1.fastq.gz	Fastqsanger.gz

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TIP5 primes prostate luminal cells for the oncogenic transformation mediated by PTEN-loss

Project description:Prostate cancer (PCa) is the second leading cause of cancer death in men. Its clinical and molecular heterogeneity and the lack of in vitro models outline the complexity of PCa in the clinical and research settings. We established an in vitro mouse PCa model based on organoid technology that takes into account the cell of origin and the order of events. Primary PCa with deletion of the tumor suppressor gene PTEN (PTEN-del) can be modeled through Pten-downregulation in mouse organoids. We used this system to elucidate the contribution of TIP5 in PCa initiation, a chromatin regulator that is implicated in aggressive PCa. High TIP5 expression correlates with primary PTEN-del PCa and this combination strongly associates with reduced PSA recurrence-free survival. TIP5 is critical for the initiation of PCa of luminal origin mediated by Pten loss whereas it is dispensable once Pten-loss mediated transformation is established. Cross-species analyses revealed a PTEN gene signature that identified a group of aggressive primary PCa characterized by PTEN-deletion, high-TIP5 expression, and a TIP5-regulated gene expression profile. The results highlight the modelling of PCa with organoids as a powerful tool to elucidate the role of genetic alterations found in recent studies in their time order and cell of origin, thereby providing further optimization for tumour stratification to improve the clinical management of PCa.

2020-02-03 | GSE131845 | GEO

TIP5 primes prostate luminal cells for the oncogenic transformation mediated by PTEN-loss.

Project description:Prostate cancer (PCa) is the second leading cause of cancer death in men. Its clinical and molecular heterogeneities and the lack of in vitro models outline the complexity of PCa in the clinical and research settings. We established an in vitro mouse PCa model based on organoid technology that takes into account the cell of origin and the order of events. Primary PCa with deletion of the tumor suppressor gene PTEN (PTEN-del) can be modeled through Pten-down-regulation in mouse organoids. We used this system to elucidate the contribution of TIP5 in PCa initiation, a chromatin regulator that is implicated in aggressive PCa. High TIP5 expression correlates with primary PTEN-del PCa and this combination strongly associates with reduced prostate-specific antigen (PSA) recurrence-free survival. TIP5 is critical for the initiation of PCa of luminal origin mediated by Pten-loss whereas it is dispensable once Pten-loss mediated transformation is established. Cross-species analyses revealed a PTEN gene signature that identified a group of aggressive primary PCas characterized by PTEN-del, high-TIP5 expression, and a TIP5-regulated gene expression profile. The results highlight the modeling of PCa with organoids as a powerful tool to elucidate the role of genetic alterations found in recent studies in their time orders and cells of origin, thereby providing further optimization for tumor stratification to improve the clinical management of PCa.

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Evaluating the effects of PTEN loss-driven cell transformation

Project description:We developed a unique in vitro transformation model utilizing PTEN CRISPR in the MCF10A human mammary epithelial cell line to study PTEN loss-induced transformation and profiled genome-wide expression in these cells to understand how PTEN loss alters the transcription landscape. We also examined changes in gene expression following inhibition of the p110b catalytic subunit of PI3 kinase, which is activated in the transformed cells. In addition, we profiled gene expression in MCF10A cells ectopically expressing PD-L1 (CD274), which is suppressed in cells harboring PTEN CRISPR.

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Epigenetic enhancer changes during oncogenic transformation

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C-tail hyperphosphorylation activates PTEN oncogenic properties

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Kim et al. STRIPAK directs PP2A activity towards MAP4K4 to promote oncogenic transformation

Project description:STRIPAK directs PP2A activity towards MAP4K4 to promote oncogenic transformation

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C-tail hyperphosphorylation activates PTEN oncogenic properties

Project description:PTEN is a multifaceted tumor suppressor that is highly sensitive to alterations in expression or function. The PTEN C-tail domain, which is rich in phosphorylation sites, has been implicated in PTEN stability, localization, catalytic activity, and protein interactions, but its role in tumor suppression remains unknown. To address this, we utilized several mouse strains with nonlethal C-tail mutations. Analysis of mice containing nonphosphorylatable or phosphomimetic versions of S380, a C-tail residue hyperphosphorylated in human gastric cancers, reveals that PTEN stability and ability to inhibit PI3K-AKT depends on dynamic phosphorylation-dephosphorylation of this residue. While phosphomimetic S380 drives neoplastic growth in prostate by promoting nuclear accumulation of β-catenin, nonphosphorylatable S380 is not tumorigenic. These data suggest that C-tail hyper-phosphorylation creates oncogenic PTEN and is a potential target for anti-cancer therapy.

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Project description:Recent studies demonstrate both basal and luminal cells of the prostate gland can initiate tumorigenesis upon oncogenic transformation. However, it remains unclear how molecular mechanisms operating within each cell lineage contribute to the initiation and progression of the prostate cancer. Here we investigate functions of individual miRNAs using genetically engineered mouse models. By both quantitative miR-Seq and in situ hybridization, we identify microRNA-205 (miR-205) as the most highly expressed miRNA and specific to the basal cells in the prostate. MicroRNA-205 expression is further elevated in the basal cells in the well-established Pten null tumorigenic mouse model. To investigate the role of miR-205 in Pten-deletion mediated tumorigenesis, we generated a Pten/miR-205 double knockout mouse model. Concurrent deletion of both miR-205 and Pten significantly compromised tumor progression in both basal and luminal compartments. We observed significantly reduced tumor size and compromised proliferation in both basal and luminal cells. We have previously demonstrated a critical requirement of miR-205 for maintaining the PI(3)K signaling and pAkt levels in skin stem cells. Consistent with this role, we observed strong reduction of pAkt and significantly increased cellular senescence in the basal cells of the dKO, compared to the Pten KO alone. These results suggest that miR-205 is cell-autonomously required for the tumorigenesis of the basal cells. Taken together, we have identified miR-205 as an important regulator in prostate cancer. Our study also reveals an essential and unexpected role of the basal cells for promoting prostate tumorigenesis.

2019-09-16 | GSE75321 | GEO

Epigenetic enhancer changes during oncogenic transformation [ChIP-seq]

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