Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA102757 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional profiling of human breast cancer cell line LM2, a subline of MDA-MB-231 highly metastatic to lung when injected to nude mice, to identify the genes that are regulated after the metastasis gene metadherin is knocked down. Keywords: Genetic modification Empty pSuper vector control cells were compared to the cells transfected with the MTDH knockdown shRNA construct. Two cultured conditions were studied: the LM2 cancer cells were cultured alone or on top of a monolayer of human lung endothelial HMVEC-L cells. Three arrays for each sample.
2010-05-26 | E-GEOD-9187 | biostudies-arrayexpress
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. The microarray was performed on three biological triplicates as well as three experimental triplictes of stable knockdown and control cells. MTDH was knocked down using a shRNA.
2010-12-17 | E-GEOD-26134 | biostudies-arrayexpress
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. The microarray was performed on three biological triplicates as well as three experimental triplicates of stable knockdown and control cells. MTDH was knocked down using a shRNA.
2011-05-01 | E-GEOD-27828 | biostudies-arrayexpress
Project description:the LM2 breast cancer cell line is an in vivo derived line from the MDA-MB-231 parental line. this LM2 line has been transduced either with a short hairpin control or miR-335 expression vector. Keywords: breast cancer, metastasis, miRNA
2008-01-01 | GSE9586 | GEO
Project description:LM2-4175 cell line was originally selected from MDA-MB-231,but has more aggressive characteristics in invasion, migration and metastasis. In addition, LM2 cell line specifically metastasizes to lung. To understand the regulatory mechanisms of lung metastasis in breast cancer, we analyzed the chromatin structure of MDA-MB-231 and LM2-4175 cell lines.
2019-07-31 | GSE124379 | GEO
Project description:Purpose: Metastatic breast cancer remains a major cause of cancer related deaths in women and there are few effective therapies against this advanced disease. Using an in vivo genetic screen, we identified WDR5 as an actionable epigenetic regulator that is required for metastatic progression in models of triple-negative breast cancer. Here we profile the transcriptome of metastatic breast cancer cells following WDR5 knockdown Methods: RNA-Seq analysis of breast cancer cell lines MDA-MB-231 LM2, BoM, BrM3 Results: We identified that WDR5 directly controls the expression of ribosomal genes. Conclusions: We found that WDR5 is a potential target in breast cancer metastasis
2022-08-31 | GSE196666 | GEO
Project description:LM2-4175 cell line was originally selected from MDA-MB-231,but has more aggressive characteristics in invasion, migration and metastasis. In addition, LM2 cell line specifically metastasizes to lung. To understand the melecular mechanisms of lung metastasis in breast cancer,we analyzed the RNA-seq data of MDA-MB-231 and LM2-4175 cell lines.
2019-07-31 | GSE124380 | GEO
Project description:Therapeutic targeting MTDH-SND1 interaction Suppresses Breast Cancer Progression and Metastasis (GSE159764). To further elucidate the tumor intrinsic effects of the targeting and the adverse effects on normal mammary epithelial cells Mouse mammary tumor cells and normal mammary epithelial cells were isolated from transgenic mouse models and cultured in vitro 3D spheroids system. MMTV-PyMT tumor cells from cKO mouse in tumorsphere culture were treaed with tamoxifen to induce Mtdh KO, and compared to the mock treatment which maintain wild type Mtdh. Thus the tumor intrinsic effects can be determined Normal mammary epithelial cells were isolated from mouse mammary gland and cultured in vitro in mammosphere. The cells were treated with inhibitor C26A6 vs control and thus the adverse effects on normal MECs can be determined.
2021-09-07 | GSE174622 | GEO
Project description:To define and compare the interactomes of the RNA binding protein HNRNPC in poorly vs. efficiently metastatic breast adenocarcinoma cells, we carried out immunoprecipitation of endogenous HNRNPC from parental MDA-MB231 cells vs. its highly metastatic isogenic derivate, the MDA-MB231-LM2 cells. We used a non-specific MOUSE IgG IP from each line as control. Each IP was performed in triplicate, and analysed by LC-MS/MS, on a Thermo Q-Exactive-plus instrument.
2023-02-19 | PXD029560 | Pride
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