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Paclitaxel resistant MDA-MB-231 Cells and resensitization with bexarotene treatment

ABSTRACT: Acquired drug resistance represents a major challenge in chemo-therapy treatment for various types of cancers. We have found that the retinoid X receptor–selective agonist bexarotene (LGD1069, Targretin) was efficacious in treating chemo-resistant cancer cells. The goal of this microarray study was to understand the mechanism of bexarotene’s role in overcoming acquired drug resistance using human breast cancer cells MDA-MB-231 as a model system and paclitaxel as model compound. After MDA-MB-231 cells were repeatedly treated with paclitaxel for 8 cycles with each cycle including a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium, MDA cells resistant to paclitaxel were developed and their growth was no longer inhibited by paclitaxel treatment. Those MDA cells with acquired drug resistance, when treated with paclitaxel and bexarotene in combination, could regain their sensitivity and their growth were again inhibited. Therefore, RNA samples from parental MDA-MB-231 cells, paclitaxel-resistant MDA cells treated with vehicle, paclitaxel alone or in combination with bexarotene, were used for perform global gene expression profiling with Affymetrix HG-U133A gene chips. Keywords: Drug Treatment

ORGANISM(S): Homo sapiens

PROVIDER: GSE12791 | GEO | 2011/07/19

SECONDARY ACCESSION(S): PRJNA112787

REPOSITORIES: GEO

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Paclitaxel resistant MDA-MB-231 Cells and resensitization with bexarotene treatment

Project description:Acquired drug resistance represents a major challenge in chemo-therapy treatment for various types of cancers. We have found that the retinoid X receptorâselective agonist bexarotene (LGD1069, Targretin) was efficacious in treating chemo-resistant cancer cells. The goal of this microarray study was to understand the mechanism of bexaroteneâs role in overcoming acquired drug resistance using human breast cancer cells MDA-MB-231 as a model system and paclitaxel as model compound. After MDA-MB-231 cells were repeatedly treated with paclitaxel for 8 cycles with each cycle including a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium, MDA cells resistant to paclitaxel were developed and their growth was no longer inhibited by paclitaxel treatment. Those MDA cells with acquired drug resistance, when treated with paclitaxel and bexarotene in combination, could regain their sensitivity and their growth were again inhibited. Therefore, RNA samples from parental MDA-MB-231 cells, paclitaxel-resistant MDA cells treated with vehicle, paclitaxel alone or in combination with bexarotene, were used for perform global gene expression profiling with Affymetrix HG-U133A gene chips. Keywords: Drug Treatment MDA-MB-231 cells were exposed to regimens on a 10-day cycle: a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium. Paclitaxel resistant MDA-MB-231 cells (MDA-PR) were established within 8 cycles of such treatment (80 days). These MDA-PR cells were then treated with vehicle control, paclitaxel along, or the combination of 30 nM paclitaxel ( 3 days on and 7 days off) and 1 ÂµM Targretin (10 days on) in a new 10-day cycle for 3 months. Thus, there are four treatment groups, parent MDA cells, MDA-PR, MDA-PR treated with paclitaxel, MDA-PR treated with paclitaxel and bexarotene, and each group had four biological replicates.

2011-07-18 | E-GEOD-12791 | biostudies-arrayexpress

Homo sapiens

Project description:Paclitaxel resistant MDA-MB-231 Cells and resensitization with bexarotene treatment

| PRJNA112787 | ENA

E-GEOD-12791

Project description:Paclitaxel resistant MDA-MB-231 Cells and resensitization with bexarotene treatment

2015-08-06 | E-GEOD-12791 | ExpressionAtlas

Gene expression data of sensitive, Docetaxel resistant and Paclitaxel resistant MDA-MB-231 Cells

Project description:The taxanes, namely Paclitaxel and Docetaxel, are important and widely used cancer chemotherapy drugs in the treatment of invasive and metastatic human breast cancer. Although treatment with the taxanes is beneficial to many patients, drug-responsive tumors in patients with metastatic breast cancer often display resistance to these drugs, either initially or over time following the continued administration of chemotherapy drugs. To investigate the patterns of cross-resistance with the taxane drugs and to identify potential mechanisms of resistance, we generated a series of MDA-MB-231 taxane resistant cell lines. We then used microarrays to determine gene expression differences between sensitive, Docetaxel and Paclitaxel resistant MDA-MB-231 cells. RNA isolated from three independent passages of sensitive, Docetaxel and Paclitaxel resistant cell lines and purified using the Qiagen RNeasy Mini Kit. Total RNA was processed and hybridized to Affymetrix Genechip HU133A arrays.

2011-04-22 | E-GEOD-28784 | biostudies-arrayexpress

Gene expression data of sensitive, Docetaxel resistant and Paclitaxel resistant MDA-MB-231 Cells

2011-04-22 | GSE28784 | GEO

Paclitaxel resistance in triple negative breast cancer involves novel functional genomic aberrations in the ABCB1 gene.

Project description:Five Triple Negative Breast Cancer cell lines were exposed to increasing concentration of Paclitaxel untill they acquired resistance. In order to identify changes in gene expression associated with resistance to PTX, we performed gene expression profiling on parental and resistant cell lines. Of ~22000 genes surveyed by microarray analysis, 5.0%, 3.7%, 9.0%, 7.3%, and 5.4% of the genes showed changes in expression of 2-fold or greater (p value < 0.05) in BT20, SUM149, MDA-MB-231, MDA-MB-436 and MDA-MB-468 cell lines, respectively.

2017-02-28 | GSE90564 | GEO

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

BCLIN25 / miRNA-125b axis regulates chemotherapeutic resistance and epithelial-mesenchymal transition

Project description:paclitaxel-resistant triple-negative breast cancer cell lines (MDA-MB-231/PTX）transfect BCLIN25-specific si-BCLIN25 to knockdown BCLIN25 and analysis differential paclitaxel-resistantlung adenocarcinoma cell lines（PC9/GR）transfect HUMT-specific shHUMT to knockdown HUMT1 and analysis differential

2021-07-06 | GSE179144 | GEO

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 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.

2012-03-01 | GSE33827 | GEO

Expression data from MDA-MB-231 cells exposed to hypoxia and/or paclitaxel or epirubicin

Project description:Hypoxia protects cancer cells from chemotherapeutic drug-induced cell death. We used microarrays to detail the changes in gene expression underlying hypoxia-induced chemoresistance in cancer cells. MDA-MB-231 were exposed to paclitaxel or epirubicin under normoxia or hypoxia for 16hours, then RNA was extracted and analyzed by Affymetrix arrays

2012-07-02 | E-GEOD-39042 | biostudies-arrayexpress

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