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A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MCF-7 breast cancer cells

ABSTRACT: The current study analyzed the metadherin (MTDH)-mediated altered gene expression profiles in ER positive MCF-7 cells. Some of these altered gene expressions were further inter connected to various pathways which may eventually be recognized as drug targets or biomarkers in those breast cancers where MTDH plays a role in cancer progression/metastasis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE59055 | GEO | 2014/09/01

SECONDARY ACCESSION(S): PRJNA254219

REPOSITORIES: GEO

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A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MCF-7 breast cancer cells

Project description:The current study analyzed the metadherin (MTDH)-mediated altered gene expression profiles in ER positive MCF-7 cells. Some of these altered gene expressions were further inter connected to various pathways which may eventually be recognized as drug targets or biomarkers in those breast cancers where MTDH plays a role in cancer progression/metastasis. To understand the global differential gene expression profile in MTDH-wild type and a newly identified MTDH-isoform knock down in malignant breast cancer cells. This data was compared to untreated breast cancer cells.

2014-09-01 | E-GEOD-59055 | biostudies-arrayexpress

A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MDA-MB-231 breast cancer cells

2014-09-01 | GSE59057 | GEO

A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MDA-MB-231 breast cancer cells

Project description:The current study analyzed the metadherin (MTDH)-mediated altered gene expression profiles in ER negative MDA-MB-231 cells. Some of these altered gene expressions were further inter connected to various pathways which may eventually be recognized as drug targets or biomarkers in those breast cancers where MTDH plays a role in cancer progression/metastasis. To understand the global differential gene expression profile in MTDH-wild type and a newly identified MTDH-isoform knock down in metastatic breast cancer cells. This data was compared to untreated breast cancer cells.

2014-09-01 | E-GEOD-59057 | biostudies-arrayexpress

A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MCF-7 breast cancer cells

| S-ECPF-GEOD-59055 | biostudies-other

A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in human breast cancer cells

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

2014-09-01 | GSE59058 | GEO

A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MDA-MB-231 breast cancer cells

| S-ECPF-GEOD-59057 | biostudies-other

A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in human breast cancer cells

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

2014-09-01 | E-GEOD-59058 | biostudies-arrayexpress

Expression data from metadherin (MTDH) knockdown in the Ishikawa H endometrial cancer cell line

Project description:Understanding the molecular underpinnings of chemoresistance is vital to design therapies to restore chemosensitivity. In particular, metadherin (MTDH) has been demonstrated to have a critical role in chemoresistance. Over-expression of MTDH has recently been implicated in poor clinical outcome in breast cancer, neroblastoma, hepatocellular carcinoma and prostate cancer. In this present study, we focused on the therapeutic benefit of MTDH depletion to restore sensitivity to cell death mediated by a combinatorial therapy of tumor necrosis factor-alpha-related apoptosis-inducing ligand (TRAIL), which promotes death of cancerous cells of the human reproductive tract, and histone deacetylase (HDAC) inhibitors, which have been shown to increase sensitivity of cancer cells to TRAIL-induced apoptosis. Our data indicate that depletion of MTDH in endometrial cancer cells results in sensitization of cells that were previously resistant to cell death mediated by combinatorial treatment with TRAIL and HDAC inhibitor LBH589. MTDH was found to be involved in G2/M checkpoint regulation in response to LBH589 alone or LBH589 in combination with TRAIL, suggesting that MTDH functions at the cell cycle checkpoint to accomplish resistance.Using microarray technology, we identified 57 downstream target genes of MTDH, including Calbindin 1 and Galectin 1, which may contribute to MTDH-mediated resistance to combinatorial TRAIL and HDAC inhibitor targeted therapy. Inhibition of PDK1,AKT phosphorylation and increase Bim expression and XIAP degradation may result in sensitivity to cell death induction in MTDH depleted Hec50co cells by TRAIL and LBH 589 combination treatment. These findings indicate that depletion of MTDH is a potentially novel avenue for effective cancer therapy.

2011-05-01 | GSE27828 | GEO

Expression data from metadherin (MTDH) knockdown in the Ishikawa H endometrial cancer cell line

2011-05-01 | E-GEOD-27828 | biostudies-arrayexpress

Cytoplasmic Miz1 Suppresses TNF-α-Induced NF-κB Activation and Hepatocellular Carcinoma Progression via the Interaction with Metadherin

Project description:Previous studies have revealed that nuclear Miz1 is implicated in the regulation of several cancers mainly relying on its POZ domain. Current study, however, uncovers an unexpected function of cytoplasmic Miz1 in hepatocellular carcinoma (HCC). In vivo HCC models in Miz1 and Miz1(POZ) KO mice along with RNA-sequencing experiments show that hepatocyte specific ablation of Miz1 exacerbates TNF-α-induced NF-κB activation and promotes the progression of HCC independent of its transcriptional activity. Ubiquitination and proteosomal degradation of cytoplasmic Miz1 liberates its novel partner Metadherin (MTDH), and its site specific phosphorylation is critical to NF-κB activation. These findings reveal a brand new role of cytosolic Miz1 as a suppressor of HCC, and provide profound insights into liver cancer diagnosis and treatment.

2020-10-11 | GSE104940 | GEO

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