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Investigate A2M treatment on human prostate cancer and mouse liver

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

OTHER RELATED OMICS DATASETS IN: PRJNA418738PRJNA416066PRJNA419257PRJNA419249

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE107195 | GEO | 2018/01/25

REPOSITORIES: GEO

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Investigate A2M treatment on human prostate cancer and mouse liver

Project description:Investigate A2M treatment on human prostate cancer and mouse liver

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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 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.

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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 on human prostate cancer xenograft in mice

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

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series