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Investigate A2M treatment on human prostate cancer and mouse liver

ABSTRACT: Investigate A2M treatment on human prostate cancer and mouse liver

OTHER RELATED OMICS DATASETS IN: GSE107195GSE107194

PROVIDER: PRJNA419249 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6297860.fastq.gz	Fastqsanger.gz
	SRR6297861.fastq.gz	Fastqsanger.gz
	SRR6297862.fastq.gz	Fastqsanger.gz
	SRR6297863.fastq.gz	Fastqsanger.gz
	SRR6297864.fastq.gz	Fastqsanger.gz

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Investigate A2M treatment in liver of mice

Project description:Investigate A2M treatment in liver of mice

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Investigate A2M treatment in liver of mice

Project description:Cancer resistance is a major cause for longevity of the naked mole-rat. Recent liver transcriptome analysis in this animal compared to wild-derived mice revealed higher expression of alpha2-macroglobulin (A2M) and cell adhesion molecules, which contribute to the naked mole-rat’s cancer resistance. Notably, A2M is known to dramatically decrease with age in humans. We hypothesize that this might facilitate tumour development. Here we found that A2M modulates tumour cell adhesion, migration and growth by inhibition of tumour promoting signalling pathways, e.g. PI3K / AKT, SMAD and up-regulated PTEN via down-regulation of miR-21, in vitro and in tumour xenografts. A2M increases the expression of CD29 and CD44 but did not evoke EMT. Transcriptome analysis of A2M-treated tumour cells, xenografts and mouse liver demonstrated a multifaceted regulation of tumour promoting signalling pathways indicating a less tumorigenic environment mediated by A2M. By virtue of these multiple actions the naturally occurring A2M has strong potential as a novel therapeutic agent.

2018-01-30 | GSE107194 | GEO

Investigate A2M treatment on human prostate cancer xenograft in mice

Project description:Investigate A2M treatment on human prostate cancer xenograft in mice

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Investigate A2M treatment on human prostate cancer xenograft in mice

Project description:Cancer resistance is a major cause for longevity of the naked mole-rat. Recent liver transcriptome analysis in this animal compared to wild-derived mice revealed higher expression of alpha2-macroglobulin (A2M) and cell adhesion molecules, which contribute to the naked mole-rat’s cancer resistance. Notably, A2M is known to dramatically decrease with age in humans. We hypothesize that this might facilitate tumor development. Here we found that A2M modulates tumor cell adhesion, migration and growth by inhibition of tumor promoting signalling pathways, e.g. PI3K / AKT, SMAD and up-regulated PTEN via down-regulation of miR-21, in vitro and in tumor xenografts. A2M increases the expression of CD29 and CD44 but did not evoke EMT. Transcriptome analysis of A2M-treated tumor cells, xenografts and mouse liver demonstrated a multifaceted regulation of tumor promoting signalling pathways indicating a less tumorigenic environment mediated by A2M. By virtue of these multiple actions the naturally occurring A2M has strong potential as a novel therapeutic agent.

2018-01-25 | GSE106989 | GEO

Investigate A2M treatment on human prostate cancer and mouse liver

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

2018-01-25 | GSE107195 | GEO

Transcriptome profiling of A2M treated A549 Cell Line Samples

Project description:The goal of the study was to identify changes in transcriptome expressions upon treatment of A549 cell line samples with activated A2M.

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Expression data from human CD34+ HPC subpopulations transduced with nuclear-trapped AF1q/MLLT11 (A2M)

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The Transcriptomic Analysis of Profibrinolytic (PLAUR) and Fibrinolytic Inhibitor (SERPINE1, A2M) Genes in COVID-19 Patients and Its Relationship with D-Dimer Levels

Project description:There is a statistically significant difference in the expression of the PLAUR and fibrinolytic inhibitor genes (SERPINE1, A2M) in mild and moderate-to-severe cases. There is a relationship between serum D-dimer levels and the expression of the PLAUR and fibrinolytic inhibitor genes (SERPINE1, A2M).

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Expression data from Notch-activated CD34+CD45RA-Lin- hematopoietic progenitor cells (HPCs) transduced with nuclear-trapped AF1q/MLLT11 (A2M)

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