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Expression data from MDA-MB-231 parental and xenograft tumor cells treated with Smac mimetic SM-164.

ABSTRACT: Small-molecule Smac mimetics target inhibitor of apoptosis (IAP) proteins to induce TNFα-dependent apoptosis in cancer cells and several Smac mimetics have been advanced into clinical development as a new class of anticancer drugs. However, preclinical studies have shown that only a small subset of cancer cell lines are sensitive to Smac mimetics used as single agents and these cell lines are at risk of developing drug resistance to Smac mimetics. Thus, it is important to understand the molecular mechanisms underlying intrinsic and acquired resistance of cancer cells to Smac mimetics in order to develop effective therapeutic strategies to overcome or prevent Smac mimetic resistance. We established Smac mimetic resistant sublines derived from MDA-MB-231 breast cancer cells, which exhibit exquisite sensitivity to the Smac mimetic SM-164, and used microarrays to detail the global programme of gene expression underlying SM-164 resistance in MDA-MB-231 cells and identified differentially expressed genes in SM-164-resistant and -sensitive MDA-MB-231 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33827 | GEO | 2012/03/01

SECONDARY ACCESSION(S): PRJNA148199

REPOSITORIES: GEO

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Expression data from MDA-MB-231 parental and xenograft tumor cells treated with Smac mimetic SM-164.

Project description:Small-molecule Smac mimetics target inhibitor of apoptosis (IAP) proteins to induce TNFÎ±-dependent apoptosis in cancer cells and several Smac mimetics have been advanced into clinical development as a new class of anticancer drugs. However, preclinical studies have shown that only a small subset of cancer cell lines are sensitive to Smac mimetics used as single agents and these cell lines are at risk of developing drug resistance to Smac mimetics. Thus, it is important to understand the molecular mechanisms underlying intrinsic and acquired resistance of cancer cells to Smac mimetics in order to develop effective therapeutic strategies to overcome or prevent Smac mimetic resistance. We established Smac mimetic resistant sublines derived from MDA-MB-231 breast cancer cells, which exhibit exquisite sensitivity to the Smac mimetic SM-164, and used microarrays to detail the global programme of gene expression underlying SM-164 resistance in MDA-MB-231 cells and identified differentially expressed genes in SM-164-resistant and -sensitive MDA-MB-231 cells. SCID mice with MDA-MB-231 xenograft tumors were treated with 5 mg/kg of SM-164 intravenously for 5 days/week for 2 weeks. SM-164-regressed MDA-MB-231 tumors regrew after treatment ended. Tumor cells from these regrown MDA-MB-231 tumors were isolated and total RNAs were prepared for microarray analysis.

2012-03-01 | E-GEOD-33827 | biostudies-arrayexpress

E-GEOD-33827

Project description:Expression data from MDA-MB-231 parental and xenograft tumor cells treated with Smac mimetic SM-164.

2015-08-18 | E-GEOD-33827 | ExpressionAtlas

Homo sapiens

Project description:Expression data from MDA-MB-231 parental and xenograft tumor cells treated with Smac mimetic SM-164.

| PRJNA148199 | ENA

Targeting of apoptotic pathways by SMAC or BH3 mimetics distinctly sensitizes paclitaxel-resistant triple negative breast cancer cells

Project description:Standard chemotherapy is the only systemic treatment for triple-negative breast cancer (TNBC). Despite the good initial responses, resistance remains a major therapeutic obstacle. Here, we employed a High-Throughput Screen to identify targeted therapies that overcome chemoresistance in TNBC. We applied short-term paclitaxel treatment and screened 320 small-molecule inhibitors of known targets to identify drugs that preferentially and efficiently target paclitaxel-treated TNBC cells. Among these compounds the SMAC mimetics (BV6, Birinapant) and BH3-mimetics (ABT-737/263) were recognized as potent targeted therapy for multiple paclitaxel-residual TNBC cell lines. However, acquired paclitaxel resistance through repeated paclitaxel pulses result in desensitization to BV6, but not to ABT-263, suggesting that short- and long-term paclitaxel resistance are mediated by distinct mechanisms. Gene expression profiling of paclitaxel-residual, -resistant and naïve MDA-MB-231 cells demonstrated that paclitaxel-residual, as opposed to -resistant cells, were characterized by an apoptotic signature, with downregulation of anti-apoptotic genes (BCL2, BIRC5), activation of apoptosis inducers (IL24, PDCD4), and enrichment of TNFα/NF-κB pathway, including upregulation of TNFSF15, coupled with cell-cycle arrest. BIRC5 and FOXM1 downregulation and IL24 induction was also evident in breast cancer patient datasets following taxane treatment. Exposure of naïve and paclitaxel-resistant cells to supernatants of paclitaxel-residual cells sensitized them to BV6, and treatment with TNFα enhanced the potency of BV6, suggesting that sensitization to BV6 is mediated, at least partially, by secreted factor(s). Our results suggest that administration of SMAC or BH3 mimetics following short-term paclitaxel treatment could be an effective therapeutic strategy for TNBC, while only BH3-mimetics could effectively overcome long-term paclitaxel resistance

2017-01-26 | GSE86839 | GEO

Tang2019 - Pharmacology modelling of AURKB and ZAK interaction in TNBC

Project description:Aurora Kinase B and ZAK interaction model Equivalent of the stochastic model used in "Network pharmacology model predicts combined Aurora B and ZAK inhibition in MDA-MB-231 breast cancer cells" by Tang et. al. 2018. The only difference is cell division and partitioning of the components, which are available in the original model for SGNS2.

2020-04-28 | BIOMD0000000940 | BioModels

Label-free mass spec analysis of human breast cancer MDA-MB-231 control cells and siICAM1 knockdown

Project description:Human breast cancer MDA-MB-231 cell siControl and siICAM1

2021-05-25 | PXD026234 | JPOST Repository

MDA-MB-231 Breast Cancer Bone Tropic vs Parental Hypoxic Secretome Analysis

Project description:The project profiled the expression patterns in hypoxia induced secretomes between MDA-MB-231 parental and MDA-MB-231 Bone Tropic (BT) breast cancer cell lines which have been previously generated by Massague and colleagues (Kang et al. Cancer Cell 2003).

2017-03-29 | MSV000080797 | MassIVE

Biomarker Profile for Prediction of Response to SMAC Mimetic Monotherapy in Pediatric Precursor B-Cell Acute Lymphoblastic Leukemia

Project description:SMAC Mimetics (SMs) are currently being evaluated in clinical trials. Biomarkers are urgently needed for prediction of patient response to SMs. This study identified a characteristic gene expression pattern of SM sensitivity suitable for upfront identification of samples with high sensitivity to SMs.

2021-11-18 | GSE140556 | GEO

RNA-seq of mesenchymal stromal cells cultured in the presence of breast cancer cell secretomes

Project description:Mesenchymal stromal cells were cultured in 3D PEG hydrogels for 7 days in the presence of serum-free media or conditioned media from a panel of breast cancer cells (MCF-7, MDA-MB-231, MDA-MB-231 lung-tropic, MDA-MB-231 brain-tropic, MDA-MB-231 bone-tropic). In all cases, the secretomes were collected after cancer cells were in serum-free media for 24h.

2019-05-28 | E-MTAB-6998 | biostudies-arrayexpress

Neuropilin-1 Knockout and Rescue Confirm its Role to Promote Metastasis in MDA-MB-231 Breast Cancer Cells

Project description:To investigate the function of Neuropilin-1 (NRP-1) in breast cancer MDA-MB-231 cells. CRISPR-Cas9 gene editing was used to knockout (KO) the NRP-1 gene in MDA-MB-231 human triple-negative breast cancer cells. Differentially expressed genes (DEGs) were determined in NRP-1 KO and parental MDA-MB-231 cells using whole transcriptome next-generation sequencing.

2023-04-11 | GSE229031 | GEO

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