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Single-cell analyses unravel cell type-specific responses to a vitamin D analogue in prostatic precancerous lesions [RNA-Seq]

ABSTRACT: We treated PTENpe-/- mice, in which PTEN is selectively ablated in prostatic epithelial cells, with a Vitamin D analog. We extracted RNA from the prostate of oil (vehicle) and Vitamin D analog-treated mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE164855 | GEO | 2021/08/04

REPOSITORIES: GEO

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Single-cell analyses unravel cell type-specific responses to a vitamin D analogue in prostatic precancerous lesions [scRNA-Seq]

Project description:Epidemiological data have linked vitamin D deficiency to the onset of various cancers, including prostate cancer, and although in-vitro studies have demonstrated anti-cancer activities for the vitamin, clinical trials provided conflicting results. To determine the impact of vitamin D signaling on prostatic precancerous lesions, we treated genetically-engineered mice harboring prostatic intraepithelial neoplasia (PIN) with Gemini-72, a vitamin D analogue with reported anti-cancer activities, and comprehensively analyzed its effects on various cell types in such lesions. We show that this analogue induces apoptosis in senescent PINs and normalizes extracellular matrix remodeling by stromal fibroblasts in an epithelial VDR-dependent manner. Furthermore, it reduces the prostatic infiltration of immunosuppressive myeloid-derived suppressor cells in an epithelial VDR-independent manner. Moreover, single-cell RNA-sequencing analysis demonstrates that while a subset of luminal epithelial cells, expressing Krt4 and Tacstd2 (termed luminal-C) with enhanced interferon signature, is lost by such a treatment, anti-apoptotic pathways are induced in persistent luminal-C cells. Therefore, our findings delineate the distinct responses of prostatic precancerous lesions and the microenvironment to the vitamin D analogue, and shed light on mechanisms that limit treatment’s efficacy.

2021-08-04 | GSE164856 | GEO

Single-cell analyses unravel cell type-specific responses to a vitamin D analogue in prostatic precancerous lesions

Project description:Single-cell analyses unravel cell type-specific responses to a vitamin D analogue in prostatic precancerous lesions

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Single-cell analyses unravel cell type-specific responses to a vitamin D analogue in prostatic precancerous lesions

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

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Single-cell analyses unravel cell type-specific responses to a vitamin D analogue in prostatic precancerous lesions [RNA-Seq]

Project description:Single-cell analyses unravel cell type-specific responses to a vitamin D analogue in prostatic precancerous lesions [RNA-Seq]

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Single-cell analyses unravel cell type-specific responses to a vitamin D analogue in prostatic precancerous lesions [scRNA-Seq]

Project description:Single-cell analyses unravel cell type-specific responses to a vitamin D analogue in prostatic precancerous lesions [scRNA-Seq]

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Single-cell analyses unravel cell type-specific responses to a vitamin D analog in prostatic precancerous lesions.

Project description:Epidemiological data have linked vitamin D deficiency to the onset and severity of various cancers, including prostate cancer, and although in vitro studies have demonstrated anticancer activities for vitamin D, clinical trials provided conflicting results. To determine the impact of vitamin D signaling on prostatic precancerous lesions, we treated genetically engineered Pten(i)pe-/- mice harboring prostatic intraepithelial neoplasia (PIN) with Gemini-72, a vitamin D analog with reported anticancer activities. We show that this analog induces apoptosis in senescent PINs, normalizes extracellular matrix remodeling by stromal fibroblasts, and reduces the prostatic infiltration of immunosuppressive myeloid-derived suppressor cells. Moreover, single-cell RNA-sequencing analysis demonstrates that while a subset of luminal cells expressing Krt8, Krt4, and Tacstd2 (termed luminal-C cells) is lost by such a treatment, antiapoptotic pathways are induced in persistent luminal-C cells. Therefore, our findings delineate the distinct responses of PINs and the microenvironment to Gemini-72, and shed light on mechanisms that limit treatment's efficacy.

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