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Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription

ABSTRACT: Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription

PROVIDER: PRJNA325721 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3662791.fastq.gz	Fastqsanger.gz
	SRR3662792.fastq.gz	Fastqsanger.gz
	SRR3662793.fastq.gz	Fastqsanger.gz
	SRR3662794.fastq.gz	Fastqsanger.gz
	SRR3662795.fastq.gz	Fastqsanger.gz

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Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription [array]

Project description:Matrix induced effects on gene expression in HeLa and MDA-MB-231 cells Tissue homeostasis is dependent on the spatially controlled localization of specific cell types and the correct composition of the extracellular stroma. While the role of the cancer stroma in tumor progression has been well characterized, the specific contribution of the matrix itself is unknown. Furthermore, the mechanisms enabling normal – not cancer – stroma to provide tumor suppressive signals and act as an anti-tumorigenic barrier are poorly understood. Here, we show that extracellular matrix (ECM) generated by normal fibroblasts (NFs) is softer than CAF-matrix and it is the physical and structural features of NF-generated matrix that regulate cancer cell proliferation . We find that normal stromal ECM triggers downregulation and nuclear exit of the histone demethylase JMJD1a resulting in the epigenetic growth restriction of carcinoma cells. Interestingly, JMJD1a positively regulates transcription of many target genes, including YAP/TAZ, and thus therefore gene expression in stiffness-dependent manner. Thus normal stromal restricts cancer cell proliferation through JMJD1a-dependent modulation of gene expression.

2016-08-29 | GSE83366 | GEO

Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription.

Project description:Tissue homeostasis is dependent on the controlled localization of specific cell types and the correct composition of the extracellular stroma. While the role of the cancer stroma in tumour progression has been well characterized, the specific contribution of the matrix itself is unknown. Furthermore, the mechanisms enabling normal-not cancer-stroma to provide tumour-suppressive signals and act as an antitumorigenic barrier are poorly understood. Here we show that extracellular matrix (ECM) generated by normal fibroblasts (NFs) is softer than the CAF matrix, and its physical and structural features regulate cancer cell proliferation. We find that normal ECM triggers downregulation and nuclear exit of the histone demethylase JMJD1a resulting in the epigenetic growth restriction of carcinoma cells. Interestingly, JMJD1a positively regulates transcription of many target genes, including YAP/TAZ (WWTR1), and therefore gene expression in a stiffness-dependent manner. Thus, normal stromal restricts cancer cell proliferation through JMJD1a-dependent modulation of gene expression.

| S-EPMC4976218 | biostudies-literature

Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription

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

2016-08-29 | GSE83370 | GEO

Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription [RNA-Seq]

Project description:gene expression data from 3 pairs of cancer associated fibroblasts and normal fibroblasts from the same individual

2016-08-29 | GSE83314 | GEO

JMJD1A inhibits proliferation and aggressiveness of gastric cancer by up-regulating RUNX3

Project description:The histone demethylase JMJD1A（Jumoji domain containing 1A） is overexpressed in multiple cancers and promotes cancer progression. However, the role and mechanism of JMJD1A in gastric cancer remains poorly understood.Here, we found that JMJD1A could suppress gastric cancer cell proliferation, migration, invasion and xenograft tumor growth. Using RNA sequencing, we identified RUNX3 as a novel target gene of JMJD1A.

2020-02-12 | GSE145105 | GEO

Homo sapiens

Project description:Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription [array]

| PRJNA325693 | ENA

Homo sapiens

Project description:Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription [RNA-Seq]

| PRJNA325541 | ENA

Jmjd1a / Jmjd2c RNAi expression profile

Project description:Global gene expression effects of silencing Jmjd1a and Jmjd2c genes We used microarrays to detail the global programme of gene expression after silencing Jmjd1a gene and Jmjd2c gene separately Keywords: dose response

2007-09-29 | GSE8937 | GEO

DNA microarray analysis of Jmjd1a and/or Jmjd1b knockout embryonic stem cells

Project description:Histone H3 lysine 9 (H3K9) methylation is an epigenetic mark of transcriptionally repressed chromatin. During mammalian development, H3K9 methylation levels seem to be spatiotemporally regulated by the opposing activities of methyltransferases and demethylases to govern correct gene expression. However, the combination(s) of H3K9 methyltransferase(s) and demethylase(s) that contribute to this regulation and the genes regulated by them remain unclear. Herein, we demonstrate the essential roles of H3K9 demethylases Jmjd1a and Jmjd1b in the embryogenesis and viability control of embryonic stem (ES) cells. Mouse embryos lacking Jmjd1a/Jmjd1b died after implantation. Depletion of Jmjd1a/Jmjd1b in mouse ES cells induced rapid cell death accompanied with a massive increase in H3K9 methylation. Jmjd1a/Jmjd1b depletion induced an increase in H3K9 methylation in the gene-rich regions of the chromosomes, indicating that Jmjd1a/Jmjd1b removes H3K9 methylation marks in the euchromatin. Importantly, the additional disruption of the H3K9 methyltransferase G9a in a Jmjd1a/Jmjd1b-deficient background rescued not only the H3K9 hypermethylation phenotype but also the cell death phenotype. We also found that Jmjd1a/Jmjd1b removes H3K9 methylation marks deposited by G9a in the Oct4 and Ccnd1 loci to activate transcription. In conclusion, Jmjd1a/Jmjd1b ensures ES cell viability by antagonizing G9a-mediated H3K9 hypermethylation in the gene-rich euchromatin.

2018-03-14 | GSE98761 | GEO

Epigenetic regulation of sex determination by the histone demethylase Jmjd1a

Project description:Developmental gene expression is defined through cross-talk between the function of transcription factors and epigenetic status including histone modification. Although several known transcription factors play crucial roles in mammalian sex determination, how chromatin regulation contributes to this process is unknown. We observed male-to-female sex reversal in mice lacking the H3K9 demethylase Jmjd1a, and found that Jmjd1a directly regulates expression of the mammalian Y chromosome sex-determining gene Sry, by regulating H3K9me2 marks. These studies reveal a pivotal role for epigenetic regulation in mammalian sex determination, and provide new impetus for identifying additional causes of disorders of sex determination by environmental factors. Gene expression patterns were measured in gonadal somatic cells of Jmjd1a mutant and control embryos at E11.5. Three biological replicates were performed in each group.

2013-08-03 | E-GEOD-49513 | biostudies-arrayexpress

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