Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA94337 | ENA |
REPOSITORIES: ENA
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Project description:Anthracycline resistance in four human cancer cell lines (HGU95A)
| PRJNA94339 | ENA
Project description:Reliable clinical tests for predicting cancer chemotherapy response are not available and individual markers failed to correctly predict resistance against anticancer agents. We hypothesized that gene expression patterns attributable to chemotherapy-resistant cells can be used as a classification tool for chemoresistance and provide novel candidate genes involved in anthracycline resistance mechanisms. We contrasted the expression profiles of 4 different human tumor cell lines of gastric, pancreatic, colon and breast origin and of their counterparts resistant to the topoisomerase inhibitors daunorubicin or doxorubicin. We also profiled the sensitive parental cells treated with doxorubicin for 24h. We interrogated Affymetrix HGU133A and U95A arrays independently. We applied two independent methods for data normalization and used Prediction Analysis of Microarrays (PAM) for feature selection. In addition, we established data sets related to drug resistance by using a “virtual array” composed of features represented on both types of oligonucleotide arrays. We identified 71 candidate genes associated with doxorubicine/daunorubicine resistance. To validate the microarray data, we also analyzed the expression of 12 selected genes by quantitative RT-PCR or immunocytochemistry, respectively. While the comparison of drug-sensitive versus drug-resistant cells yields candidates associated with drug resistance, the 24h treatment of sensitive parental cells produced a distinct transcriptional profile related to short-term drug effects. Keywords: superSeries This reference Series links data in the following related Series: GSE3926 Anthracycline treatment and resistance in four human cancer cell lines (HGU133A) GSE3927 Anthracycline resistance in four human cancer cell lines (HGU95A)
2010-04-14 | E-GEOD-3929 | biostudies-arrayexpress
Project description:Drug resistance in breast cancer is the major obstacle to a successful outcome following chemotherapy treatment. While upregulation of multidrug resistance (MDR) genes is a key component of drug resistance in multiple cancers, the complexity and hierarchy of non-MDR driven drug resistance pathways are still largely unknown. The aim of this study was to identify pathways contributing to anthracycline resistance using isogenic drug resistant breast cancer cell lines. We generated isogenic MDA-MB-231, MCF7, SKBR3 and ZR-75-1 epirubicin-resistant breast cancer cell lines, which were cross-resistant to doxorubicin and SN-38; the SKBR3 cell line was also resistant to taxanes. Epirubicin-resistant cells were morphologically different from native cells, and had alterations in apoptosis and cell cycle profile. Using gene expression and small-molecule inhibitor analyses we identified deregulation of histone H2A and H2B genes in all four cell lines. These genes contribute to several biological pathways, which include cell cycle, chromosomal maintenance, epigenetics, RNA and mitochondrial transcription. Histone deacetylase and cell cycle/DNA damage small molecule inhibitors reversed resistance and were cytotoxic for all four epirubicin-resistant cell lines confirming that histone and cell cycle pathways are associated with epirubicin resistance. This study has established model systems for investigating drug resistance in all four breast cancer subtypes and revealed key pathways that contribute to anthracycline resistance. The global gene expression analysis included 4 parental (anthracycline sensitive) and 4 resistant breast cancer cell lines, in biological triplicates.
2014-01-24 | E-GEOD-54326 | biostudies-arrayexpress
Project description:Drug resistance in breast cancer is the major obstacle to a successful outcome following chemotherapy treatment. While upregulation of multidrug resistance (MDR) genes is a key component of drug resistance in multiple cancers, the complexity and hierarchy of non-MDR driven drug resistance pathways are still largely unknown. The aim of this study was to identify pathways contributing to anthracycline resistance using isogenic drug resistant breast cancer cell lines. We generated isogenic MDA-MB-231, MCF7, SKBR3 and ZR-75-1 epirubicin-resistant breast cancer cell lines, which were cross-resistant to doxorubicin and SN-38; the SKBR3 cell line was also resistant to taxanes. Epirubicin-resistant cells were morphologically different from native cells, and had alterations in apoptosis and cell cycle profile. Using gene expression and small-molecule inhibitor analyses we identified deregulation of histone H2A and H2B genes in all four cell lines. These genes contribute to several biological pathways, which include cell cycle, chromosomal maintenance, epigenetics, RNA and mitochondrial transcription. Histone deacetylase and cell cycle/DNA damage small molecule inhibitors reversed resistance and were cytotoxic for all four epirubicin-resistant cell lines confirming that histone and cell cycle pathways are associated with epirubicin resistance. This study has established model systems for investigating drug resistance in all four breast cancer subtypes and revealed key pathways that contribute to anthracycline resistance.
2014-01-24 | GSE54326 | GEO
Project description:Global gene expression analysis of anthracycline-resistant breast cancer cell lines
| PRJNA236203 | ENA
Project description:MRNA expression data from human breast cancer cell lines after demethylation treatment.
| PRJNA142857 | ENA
Project description:MicroRNA expression data from human breast cancer cell lines after demethylation treatment.
| PRJNA142859 | ENA
Project description:Neoadjuvant chemotherapy (NAC) is the major pre-treatment for breast cancer before surgery. Patients who achieve pathologic complete response (pCR) have a higher chance to receive lumpectomy and a better quality of life after neoadjuvant treatment. Luminal subtype breast cancer has poor NAC response compared with triple-negative breast cancer (TNBC) subtype. The molecular and cellular mechanisms underlying this chemoresistance are not fully understood. Here we report that the 17 featured transcriptional factors (TFs) in luminal and TNBC were identified. The association between 17 TFs and NAC pCR were analysis and exogenous luminal featured TF GATA3 overexpression promotes chemotherapy resistance in TNBC cell lines whereas its knockdown promotes sensitivity. In mechanism, we found that anthracycline based chemotherapy induces robust cellular ROS and Fe2+ overload in sensitivity cells; GATA3 mediates cell survival through repress CYB5R2 expression and Fenton reducing in DOX recycle which reduce cellular ROS and Fe2+ level during chemotherapy procedure. These founding altogether indicate that luminal featured transcription factor GATA3 enhance NAC resistance thorough repress ROS production and Fenton reducing. Breast cancer patient with GATA3 high expression might not suit for anthracycline based NAC regimen.
2023-01-01 | GSE216413 | GEO