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Clinical significance of MSP-RON signaling based on mRNA-microRNA integration analyses in acute severe ischemic stroke patients (mRNA data)

ABSTRACT: Clinical significance of MSP-RON signaling based on mRNA-microRNA integration analyses in acute severe ischemic stroke patients (mRNA data)

PROVIDER: PRJNA836429 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19142079_1.fastq.gz	Fastqsanger.gz
	SRR19142079_2.fastq.gz	Fastqsanger.gz
	SRR19142080_1.fastq.gz	Fastqsanger.gz
	SRR19142080_2.fastq.gz	Fastqsanger.gz
	SRR19142081_1.fastq.gz	Fastqsanger.gz

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Clinical significance of MSP-RON signaling based on mRNA-microRNA integration analyses in acute severe ischemic stroke patients

Project description:Clinical significance of MSP-RON signaling based on mRNA-microRNA integration analyses in acute severe ischemic stroke patients

| PRJNA837080 | ENA

Functional Comparison of the HGF/Met and MSP/Ron Systems in a Pancreatic Cancer Model

Project description:Pancreatic cancer is an aggressive disease with a poor prognosis for which current standard chemotherapeutic treatment options offer little survival benefit. In recent years, receptor tyrosine kinases (RTK)s have garnered interest as therapeutic targets to augment or replace standard chemotherapeutic therapies because of their high expression levels in various cancers and their ability to promote cell growth, migration, and survival. Met and Ron, which are homologous RTKs activated by the ligands hepatocyte growth factor (HGF) and macrophage stimulating protein (MSP), respectively, are over-activated in many of the least treatable cancers. In pancreatic adenocarcinoma, Met expression is linked to poor patient survival and Ron expression is generally higher in tumor samples relative to normal tissue, although its prognostic significance in pancreatic cancer remains unclear. Despite the structural homology between Met and Ron, studies that have directly compared the functional outcomes of these systems in any context are limited. To address this, we sought to determine if the HGF/Met and MSP/Ron systems produce overlapping or divergent contributions towards a malignant phenotype by performing a characterization of MSP and HGF driven signaling, behavioral, and transcriptomic responses in pancreatic cancer cells in vitro. We found HGF and MSP both encouraged cell migration and activated the MAPK/Erk pathway both at the transcript and protein level. HGF uniquely increased proliferation in addition to regulating a wider variety of transcripts compared to MSP. Although HGF and MSP produced a differing breadth of responses, overlapping pro-cancer signaling, behavioral, and transcriptional effects suggest dual inhibition of the MSP/Ron and HGF/Met systems in pancreatic cancer may provide a more complete anti-cancer effect compared to individually targeting either system.

2019-06-14 | GSE129075 | GEO

Clinical significance of MSP-RON signaling based on mRNA-microRNA integration analyses in acute severe ischemic stroke patients (micro RNA data)

Project description:Clinical significance of MSP-RON signaling based on mRNA-microRNA integration analyses in acute severe ischemic stroke patients (micro RNA data)

| PRJNA837084 | ENA

Clinical significance of MSP-RON signaling based on mRNA-microRNA integration analyses in acute severe ischemic stroke patients (mRNA data)

Project description:The roles of mRNA and microRNA (miRNA) are widely known in many diseases including acute ischemic stroke. About 60 % of all human messenger RNAs (mRNAs) are regulated by microRNAs. Integration analysis using mRNA and miRNA are important to elucidate pathogenesis. But the contribution of mRNA and miRNA, especially miRNA targeted mRNA, related with severity of acute ischemic stroke is not remain understood. To clarify the pathway related with the severity of acute ischemic stroke, we examined mRNA and miRNA integration analysis targeted for acute ischemic stroke.

2023-08-11 | GSE202518 | GEO

Clinical significance of MSP-RON signaling based on mRNA-microRNA integration analyses in acute severe ischemic stroke patients (micro RNA data)

2023-08-11 | GSE202708 | GEO

The RON receptor tyrosine kinase promotes metastasis by triggering epigenetic reprogramming through the thymine glycosylase MBD4 (Bisulfite-Seq)

Project description:Metastasis is the major cause of death in cancer patients, yet the genetic/epigenetic programs that drive metastasis are poorly understood. Here, we report a novel epigenetic reprogramming pathway that is required for breast cancer metastasis. Concerted differential DNA methylation is initiated by activation of the RON receptor tyrosine kinase by its ligand, macrophage stimulating protein (MSP). Through PI3K signaling, RON/MSP promotes expression of the G:T mismatch-specific thymine glycosylase MBD4. RON/MSP and MBD4-dependent aberrant DNA methylation results in misregulation of a specific set of genes. Knockdown of MBD4 reverses methylation at these specific loci, and blocks metastasis. We also show that the MBD4 glycosylase catalytic residue is required for RON/MSP-driven metastasis. Analysis of human breast cancers using a set of specific genes that are regulated by RON/MSP through MBD4-directed aberrant DNA methylation revealed that this epigenetic program is significantly associated with poor clinical outcome. Furthermore, inhibition of Ron kinase activity with a new pharmacological agent prevents activation of the RON/MBD4 pathway and blocks metastasis of patient-derived breast tumor grafts in vivo.

2014-01-02 | GSE52688 | GEO

The RON receptor tyrosine kinase promotes metastasis by triggering epigenetic reprogramming through the thymine glycosylase MBD4 (RNA-Seq)

2014-01-02 | GSE52687 | GEO

Clinical significance of MSP-RON signaling based on mRNA-microRNA integration analyses in acute severe ischemic stroke patients

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

2023-08-13 | GSE202709 | GEO

The RON receptor tyrosine kinase promotes metastasis by triggering epigenetic reprogramming through the thymine glycosylase MBD4 (gene expression array)

Project description:Metastasis is the major cause of death in cancer patients, yet the genetic/epigenetic programs that drive metastasis are poorly understood. Here, we report a novel epigenetic reprogramming pathway that is required for breast cancer metastasis. Concerted differential DNA methylation is initiated by activation of the RON receptor tyrosine kinase by its ligand, macrophage stimulating protein (MSP). Through PI3K signaling, RON/MSP promotes expression of the G:T mismatch-specific thymine glycosylase MBD4. RON/MSP and MBD4-dependent aberrant DNA methylation results in misregulation of a specific set of genes. Knockdown of MBD4 reverses methylation at these specific loci, and blocks metastasis. We also show that the MBD4 glycosylase catalytic residue is required for RON/MSP-driven metastasis. Analysis of human breast cancers revealed that this epigenetic program is significantly associated with poor clinical outcome. Furthermore, inhibition of Ron kinase activity with a new pharmacological agent blocks metastasis of patient-derived breast tumor grafts in vivo. To determine the molecular mechanisms by which RON/MSP drives breast cancer metastasis, we performed microarray gene expression profiling of MCF7, MCF7-RON/MSP and MCF7-RON/MSP-shMBD4 cells.

2014-01-02 | E-GEOD-52567 | biostudies-arrayexpress

The RON receptor tyrosine kinase promotes metastasis by triggering epigenetic reprogramming through the thymine glycosylase MBD4 (gene expression array)

Project description:Metastasis is the major cause of death in cancer patients, yet the genetic/epigenetic programs that drive metastasis are poorly understood. Here, we report a novel epigenetic reprogramming pathway that is required for breast cancer metastasis. Concerted differential DNA methylation is initiated by activation of the RON receptor tyrosine kinase by its ligand, macrophage stimulating protein (MSP). Through PI3K signaling, RON/MSP promotes expression of the G:T mismatch-specific thymine glycosylase MBD4. RON/MSP and MBD4-dependent aberrant DNA methylation results in misregulation of a specific set of genes. Knockdown of MBD4 reverses methylation at these specific loci, and blocks metastasis. We also show that the MBD4 glycosylase catalytic residue is required for RON/MSP-driven metastasis. Analysis of human breast cancers revealed that this epigenetic program is significantly associated with poor clinical outcome. Furthermore, inhibition of Ron kinase activity with a new pharmacological agent blocks metastasis of patient-derived breast tumor grafts in vivo.

2014-01-02 | GSE52567 | GEO

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