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Single Cell Analysis Reveals The Essential Role of TGFbeta Pathway in Shaping Immune-suppressive Microenvironment and Promoting CRPC Development

ABSTRACT: To understand the dynamic changes of different cell populations within the Pten-null prostate cancer model in response to ADT, we carried out scRNA-seq transcriptome analysis on CD45- and CD45+ FACS-sorted cells from Pten-null intact (CP), early-(CRPC-4wks) and late-(CRPC-12wks) stage castrated prostates, respectively. To systematically investigate the effects of androgen deprivation therapy (ADT) on the cellular landscapes of primary and CRPC as well as intra- and extra-tumoral immune cells and their functional status at single cell level, we conducted scRNA-seq on CD45+ cells from bone marrow, blood, spleen and thymus of intact, early- and late-stage castrated Pten-null mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE270744 | GEO | 2025/06/18

REPOSITORIES: GEO

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Single Cell Analysis Reveals The Essential Role of TGFbeta Pathway in Shaping Immune-suppressive Microenvironment and Promoting CRPC Development (bulk RNA-Seq)

Project description:To understand the dynamic changes of different cell populations within the Pten-null prostate cancer model in response to ADT, we carried out scRNA-seq transcriptome analysis on CD45- and CD45+ FACS-sorted cells from Pten-null intact (CP), early-(nmCRPC-4wks) and late-(nmCRPC-12wks) stage castrated prostates, respectively. To systematically investigate the effects of androgen deprivation therapy (ADT) on the cellular landscapes of primary and nmCRPC as well as intra- and extra-tumoral immune cells and their functional status at single cell level, we conducted scRNA-seq on CD45+ cells from bone marrow, blood, spleen and thymus of intact, early- and late-stage castrated Pten-null mice.

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Schlafen family member 5 (SLFN5) regulates LAT1-mediated mTOR activation in castration-resistant prostate cancer (PART 2)

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Project description:Alteration of the PTEN/PI3K pathway is associated with late stage and castrate resistant prostate cancer (CRPC). However, how PTEN loss involves in CRPC development is not clear. Here we show that castration-resistant growth is an intrinsic property of Pten-null prostate cancer (CaP) cells, independent of cancer development stage.PTEN loss suppresses androgen-responsive gene expressions by modulating androgen receptor (AR) transcription factor activity. Conditional deletion of AR in the epithelium promotes the proliferation of Pten-null cancer cells, at least in part, by down-regulating androgen-responsive gene FKBP5 and preventing PHLPP-mediated AKT inhibition. Our findings identify PI3K and AR pathway crosstalk as a mechanism of CRPC development, with potentially important implications for CaP etiology and therapy Mouse embryonic fibroblasts (MEFs) carrying a tet-inducible Pten transgene were generated by retro viral infection and antibiotic selection. Cells were treated with 2 ug/ml doxycycline for 24 or 48 hours in tet-free FBS (5%)/MEF media (n=2). Reference samples were either cells before treatment (n=2). After each time point cells were washed twice with PBS and RNA trizol extracted. WT samples (n =2) were also included as a control.

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Mus musculus

Project description:PTEN intact and NULL prostates in intact and castrate mice.

| PRJNA132265 | ENA

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