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

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

PROVIDER: PRJNA681285 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13160971.fastq.gz	Fastqsanger.gz
	SRR13160972.fastq.gz	Fastqsanger.gz
	SRR13160973.fastq.gz	Fastqsanger.gz
	SRR13160974.fastq.gz	Fastqsanger.gz
	SRR13160975.fastq.gz	Fastqsanger.gz

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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

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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 (ATAC-seq)

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

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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

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

2022-01-20 | GSE162294 | GEO

Mechanism of TP53 and RB1 inactivation-induced neuroendocrine phenotype transformation in TKI-resistant lung adenocarcinoma

Project description:In order to study the mechanism of co-inactivation of RB1 and TP53 in the transformation of lung adenocarcinoma to small cell lung cancer, we established the NCI-H1975 cell line with RB1 knockdown.NCI-H1975 cells were cultured and infected with lentivirus expressing RB1-shRNA (n=3) or pLKO.1-shRNA (n=3), We then performed transcriptome sequencing (RNA-seq) on the above cells.

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Involvement of ERK, Wnt and BMP2 signaling in human articular chondrocyte dedifferentiation in monolayer culture

Project description:Objective: When primary chondrocytes are cultured in monolayer, they undergo dedifferentiation during which they lose their phenotype and their capacity to form cartilage. Dedifferentiation is an obstacle for cell therapy for cartilage degeneration. In this study, we aimed to systemically evaluate the changes in gene expression during dedifferentiation of human articular chondrocytes to identify underlying mechanisms. Methods: RNA was isolated from monolayer-cultured primary human articular chondrocytes at serial passages. Gene expression was analyzed by microarray. Based on the microarray analysis, relevant genes and pathways were identified. Their functions in chondrocyte dedifferentiation were further investigated in detail. Results: In vitro expanded human chondrocytes showed progressive changes in gene expression during dedifferentiation. Strikingly, an overall decrease in total gene expression was detected. Genes in the Wnt and BMP pathways exhibited significant changes in expression. The non-canonical rather than the canonical Wnt pathway was found to be involved in the loss of collagen II synthesis. BMP2 was able to decelerate the dedifferentiation and reinforce the maintenance of chondrocyte phenotype in monolayer culture. DNA methylation was in part responsible for the expression downregulation of a set of genes. Conclusion: Our study revealed the roles of ERK, Wnt and BMP pathways as well as DNA methylation in chondrocyte dedifferentiation in monolayer culture. RNA human chondrocytes were allowed to dedifferentiate for 8 passages. RNA was isolated at week 0, 2 ,4, 6 and 8, which was subjected to whole genome gene expression analysis.

2012-11-14 | E-GEOD-42235 | biostudies-arrayexpress

Involvement of ERK, Wnt and BMP2 signaling in human articular chondrocyte dedifferentiation in monolayer culture

2012-11-14 | GSE42235 | GEO