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Transcriptional Inactivation of TP53 and BMP Pathway Components Mediates Therapy-induced Dedifferentiation and Metastasis in Prostate Cancer (RNA-seq)

ABSTRACT: AR blockade instigates two separate and complementary processes: 1) transcriptional silencing of TP53 and hence acquisition of hybrid E/M and stem-like traits; and 2) inhibition of the BMP signaling, which promotes resistance to the pro-apoptotic and anti-proliferative effects of AR inhibition. The drug tolerant prostate cancer cells generated through reprogramming are rescued by neuregulin and generate metastases in mice.

ORGANISM(S): Homo sapiens

PROVIDER: GSE162225 | GEO | 2022/01/20

REPOSITORIES: GEO

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Transcriptional Inactivation of TP53 and BMP Pathway Components Mediates Therapy-induced Dedifferentiation and Metastasis in Prostate Cancer (ChIP-seq)

Project description:AR blockade instigates two separate and complementary processes: 1) transcriptional silencing of TP53 and hence acquisition of hybrid E/M and stem-like traits; and 2) inhibition of the BMP signaling, which promotes resistance to the pro-apoptotic and anti-proliferative effects of AR inhibition. The drug tolerant prostate cancer cells generated through reprogramming are rescued by neuregulin and generate metastases in mice.

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Transcriptional Inactivation of TP53 and BMP Pathway Components Mediates Therapy-induced Dedifferentiation and Metastasis in Prostate Cancer

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

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Transcriptional Inactivation of TP53 and BMP Pathway Components Mediates Therapy-induced Dedifferentiation and Metastasis in Prostate Cancer

Project description:Transcriptional Inactivation of TP53 and BMP Pathway Components Mediates Therapy-induced Dedifferentiation and Metastasis in Prostate Cancer

| PRJNA681284 | ENA

Transcriptional Inactivation of TP53 and BMP Pathway Components Mediates Therapy-induced Dedifferentiation and Metastasis in Prostate Cancer (RNA-seq)

Project description:Transcriptional Inactivation of TP53 and BMP Pathway Components Mediates Therapy-induced Dedifferentiation and Metastasis in Prostate Cancer (RNA-seq)

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Transcriptional Inactivation of TP53 and BMP Pathway Components Mediates Therapy-induced Dedifferentiation and Metastasis in Prostate Cancer (ChIP-seq)

Project description:Transcriptional Inactivation of TP53 and BMP Pathway Components Mediates Therapy-induced Dedifferentiation and Metastasis in Prostate Cancer (ChIP-seq)

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Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding

Project description:Insufficient insulin secretion is a hallmark of type 2 diabetes and has been attributed to beta cell identity loss characterized by a decreased expression of several key beta cell genes. The pro-inflammatory factor BMP-2 is upregulated in islets of Langerhans from diabetic individuals and acts as an inhibitor of beta cell function and proliferation. Exposure to BMP-2 induces expression of Id1-4, Hes-1 and Hey-1, transcriptional regulators associated with loss of differentiation. The aim of this study was to investigate the mechanism of BMP-2 induced beta cell dysfunction and identity loss. Mouse islets exposed to BMP-2 for 10 days showed impaired insulin secretion and beta cell proliferation. BMP-2-induced beta cell dysfunction was associated with decreased expression of beta cell specific identity and proliferation markers such as Ins1, Ucn3 and Ki67 but increased expression of Id1-4, Hes-1 and Hey-1. BMP-2 regulated mRNA expression significantly correlated with corresponding protein expression. BMP-2 induced gene expression changes were associated with a predominant reduction in the H3K27ac mark and a decrease in NeuroD1 chromatin binding activity. These results show that BMP-2-induced beta cell dysfunction is associated with epigenetic changes, predominantly a reduction in H3K27ac and a decrease in NeuroD1 DNA binding resulting in altered beta cell gene expression.

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Autocrine BMP-4 signaling promotes survival of colorectal cancer cells.

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Genome-wide analysis of endocytosis inhibition on BMP-2 induced gene expression in C2C12 cells

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