Transcriptional changes in the breast cancer cell line MCF7 rendered resistant to the cationic drug siramesine
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ABSTRACT:
PROVIDER: PRJNA539897 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8962155.fastq.gz | Fastqsanger.gz | |||
| SRR8962156_1.fastq.gz | Fastqsanger.gz | |||
| SRR8962156_2.fastq.gz | Fastqsanger.gz | |||
| SRR8962157.fastq.gz | Fastqsanger.gz | |||
| SRR8962158_1.fastq.gz | Fastqsanger.gz |
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Project description:Repurpusing cationic amphiphilic drugs (CADs) may be enhance the effect of chemotherapy in cancer treatment. In order to understand the molecular mechanism, we created cell lines resistant to the CAD siramesine by growing them for 6 months in increasing concentrations of siramesine. Parental and resistant cell lines were subjected to RNAseq and revealed diffentially expressed genes in ca+ and cAMP signalling pathways.
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Project description:10X Genomics single cell RNAseq of MCF7 cells Human cancer cell lines are the workhorse of cancer research. While cell lines are known to evolve in culture, the extent of the resultant genetic and transcriptional heterogeneity and its functional consequences remain understudied. Here, genomic analyses of 106 cell lines grown in two laboratories revealed extensive clonal diversity. Follow-up comprehensive genomic characterization of 27 strains of the common breast cancer cell line MCF7 uncovered rapid genetic diversification. Similar results were obtained with multiple strains of 13 additional cell lines. Importantly, genetic changes were associated with differential activation of gene expression programs and marked differences in cell morphology and proliferation. Barcoding experiments showed that cell line evolution occurs as a result of positive clonal selection that is highly sensitive to culture conditions. Analyses of single cell-derived clones showed that ongoing instability quickly translates into cell line heterogeneity. Testing of the 27 MCF7 strains against 321 anti-cancer compounds uncovered strikingly disparate drug response: at least 75% of compounds that strongly inhibited some strains were completely inactive in others. This study documents the extent, origin and consequence of genetic variation within cell lines, and provides a framework for researchers to measure such variation in efforts to support maximally reproducible cancer research.
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Project description:To investigate the effect of FOXK2 knockdown on transcriptomic profiling in breast cancer and delineate the role of FOXK2 in breast cancer growth. We knockdowned the gene exprssion of FOXK2 in MCF7 cells and performed gene expression profiling analysis using data obtained from RNA-seq.
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Project description:Identification of TRPS1 interactors in MCF7 breast cancer cell line.
2018-07-17 | PXD010312 | Pride
Project description:10X Genomics single cell RNAseq of MCF7 cells treated with bortezomib. Human cancer cell lines are the workhorse of cancer research. While cell lines are known to evolve in culture, the extent of the resultant genetic and transcriptional heterogeneity and its functional consequences remain understudied. Here, genomic analyses of 106 cell lines grown in two laboratories revealed extensive clonal diversity. Follow-up comprehensive genomic characterization of 27 strains of the common breast cancer cell line MCF7 uncovered rapid genetic diversification. Similar results were obtained with multiple strains of 13 additional cell lines. Importantly, genetic changes were associated with differential activation of gene expression programs and marked differences in cell morphology and proliferation. Barcoding experiments showed that cell line evolution occurs as a result of positive clonal selection that is highly sensitive to culture conditions. Analyses of single cell-derived clones showed that ongoing instability quickly translates into cell line heterogeneity. Testing of the 27 MCF7 strains against 321 anti-cancer compounds uncovered strikingly disparate drug response: at least 75% of compounds that strongly inhibited some strains were completely inactive in others. This study documents the extent, origin and consequence of genetic variation within cell lines, and provides a framework for researchers to measure such variation in efforts to support maximally reproducible cancer research.
2018-08-01 | GSE114461 | GEO
Project description:10X Genomics single cell RNAseq of MCF7 cells Human cancer cell lines are the workhorse of cancer research. While cell lines are known to evolve in culture, the extent of the resultant genetic and transcriptional heterogeneity and its functional consequences remain understudied. Here, genomic analyses of 106 cell lines grown in two laboratories revealed extensive clonal diversity. Follow-up comprehensive genomic characterization of 27 strains of the common breast cancer cell line MCF7 uncovered rapid genetic diversification. Similar results were obtained with multiple strains of 13 additional cell lines. Importantly, genetic changes were associated with differential activation of gene expression programs and marked differences in cell morphology and proliferation. Barcoding experiments showed that cell line evolution occurs as a result of positive clonal selection that is highly sensitive to culture conditions. Analyses of single cell-derived clones showed that ongoing instability quickly translates into cell line heterogeneity. Testing of the 27 MCF7 strains against 321 anti-cancer compounds uncovered strikingly disparate drug response: at least 75% of compounds that strongly inhibited some strains were completely inactive in others. This study documents the extent, origin and consequence of genetic variation within cell lines, and provides a framework for researchers to measure such variation in efforts to support maximally reproducible cancer research.
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Project description:The second leading cause of cancer death for women in the U.S. is breast cancer. Moreover, a significant number of patients with breast tumors acquire resistance to drugs during therapy. To develop targeted therapeutic strategies to combat drug resistance it is essential to understand the basic molecular mechanisms through which cancer cells control sensitivity to chemotherapeutics. To identify new candidate genes and facilitate the discovery of novel drug resistance pathways, we have generated a resistance profile or âresistomeâ of etoposide resistant MCF7 breast cancer cells. Differential expression of over 5000 genes (fold change > 2, P value < 0.05) indicate that several drug resistance mechanisms may be operating in these cells, including up-regulation of ABC transporter genes, down-regulation of the drug target and down-regulation of apoptotic genes. Several transcription factors such as RUNX2, SOX9, ETS1 and SMAD3 were up-regulated in the drug resistant cells. Targeted RUNX2 knockdown in the resistant cells using siRNA increased sensitivity to etoposide and also upregulated expression of pro-apoptotic genes indicating that RUNX2 could be a molecular target against etoposide resistance. Differential miRNA (microRNA) expression was observed among the drug resistant and sensitive cells suggesting that miRNA may also play a role in regulation of drug resistance. Hsa-miR-218, which targets ABCC6, was down-regulated in the drug resistant cell line. Transfection of a miR-218 mimic could down-regulate the expression of the efflux pump ABCC6 by 65% in drug resistant cells suggesting that regulation of miRNA may play an important role in etoposide resistance. RNA from MCF7 and etoposide-resistant MCF7 (MCF7VP) cell lines were hybridized to Affymetrix microarrays. Both samples were run in triplicate
2011-04-08 | E-GEOD-28413 | biostudies-arrayexpress
Project description:The MCF7 cell line represents a typical epithelial cell line and corresponds to luminal A breast cancer (estrogen-responsive). Overexpression of HAX1 was demonstrated in MCF7 cell line as well as in breast cancer samples, suggesting a role of HAX1 in breast cancer progression. HAX1 is a 32-kDa protein of unknown structure, involved in the regulation of apoptosis, cell migration and calcium homeostasis. It was also shown to bind mRNA. Scarcity of structural elements and the presence of a disordered region, inferred from HAX1 sequence, suggests that HAX1 is intrinsically disordered, and may have many protein-protein interactions. So far about 40 different proteins were characterized as HAX1 protein partners. In the present work, applying immunoaffinity chromatography coupled with mass spectrometry, we identified new candidates for HAX1 binding partners in breast cancer cells. Newly identified proteins may be divided into three, partially overlapping groups: cytoskeleton-associated proteins, GTP-ase associated proteins and RNA-binding proteins. These results imply that HAX1 has more protein partners than hitherto described. Subsequent analysis of these interactions may shed some light into molecular mechanisms of HAX1 functions.
2019-11-14 | PXD007888 | Pride