MicroRNAs expression data from two different types of human breast cancer cells
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ABSTRACT:
ORGANISM(S): synthetic construct Homo sapiens
PROVIDER: GSE96821 | GEO | 2017/03/21
SECONDARY ACCESSION(S): PRJNA379820
REPOSITORIES: GEO
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2020-06-01 | GSE141698 | GEO
Project description:Chemoresistance in breast cancer has been a great interest in past studies, however, the development of rational therapeutic strategies targeting chemoresistant cells is still a challenge for clinical oncology.The resistant property of MCF7/ADR cells was confirmed by long term culture with Dox, cell viability, and PARP cleavage assays. Microarray analysis was performed to compare the global differences of gene expression between MCF-7 and MCF-7/ADR cells. MCF-7 and MCF-7/ADR gene expression profiles were analyzed. Total RNA were prepared for analysis with Affymetrix Human U133 Plus 2.0 arrays according to the manufacturerâs instructions.
2016-01-05 | E-GEOD-76540 | biostudies-arrayexpress
Project description:Worldwide, breast cancer (BRCA) is the most common malignant tumor in women. Adriamycin (ADR) is considered one of the most effective agents for the treatment of BRCA, but its efficacy as a curative agent is compromised by intrinsic resistance and the acquisition of multidrug resistance characteristics during chemotherapy. The underlying mechanisms resulting in ADR resistance in BRCA remain poorly understood. Long non-coding RNA (lncRNA) are abnormally expressed in many cancers and are highly involved in its pathogenesis, including drug resistance. In order to systematically study the role of lncRNA in the resistance of BRCA cells to ADR, we used lncRNA expression microarray to establish gene expression profiles of ADR resistant cell lines and ADR sensitive cell lines.
2020-08-01 | GSE155478 | GEO
Project description:Chemoresistance in breast cancer has been a great interest in past studies, however, the development of rational therapeutic strategies targeting chemoresistant cells is still a challenge for clinical oncology.The resistant property of MCF7/ADR cells was confirmed by long term culture with Dox, cell viability, and PARP cleavage assays. Microarray analysis was performed to compare the global differences of gene expression between MCF-7 and MCF-7/ADR cells.
2016-01-05 | GSE76540 | GEO
Project description:Background: Cancer stem cells are presumed to have virtually unlimited proliferative and self-renewal abilities and to be highly resistant to chemotherapy, a feature that is associated with overexpression of ATP-binding cassette transporters. We investigated whether prolonged continuous selection of cells for drug resistance enriches cultures for cancer stem-like cells. Methods: Cancer stem cells were defined as CD44+/CD24– cells that could self-renew (ie, generate cells with the tumorigenic CD44+/CD24– phenotype), differentiate, invade, and form tumors in vivo. We used doxorubicin-selected MCF-7/ADR cells, weakly tumorigenic parental MCF-7 cells, and MCF-7/MDR, an MCF-7 subline with forced expression of ABCB1 protein. Cells were examined for cell surface markers and side-population fractions by microarray and flow cytometry, with in vitro invasion assays, and for ability to form mammospheres. Xenograft tumors were generated in mice to examine tumorigenicity (n = 52). The mRNA expression of multidrug resistance genes was examined in putative cancer stem cells and pathway analysis of statistically significantly differentially expressed genes was performed. All statistical tests were two-sided. Results: Pathway analysis showed that MCF-7/ADR cells express mRNAs from ABCB1 and other genes also found in breast cancer stem cells (eg, CD44, TGFB1, and SNAI1). MCF-7/ADR cells were highly invasive, formed mammospheres, and were tumorigenic in mice. In contrast to parental MCF-7 cells, more than 30% of MCF-7/ADR cells had a CD44+/CD24– phenotype, could self-renew, and differentiate (ie, produce CD44+/CD24– and CD44+/CD24+ cells), and overexpressed various multidrug resistance-linked genes (including ABCB1, CCNE1, and MMP9). MCF-7/ADR cells were statistically significantly more invasive in Matrigel than parental MCF-7 cells (MCF-7 cells = 0.82 cell per field and MCF-7/ADR = 7.51 cells per field, difference = 6.69 cells per field, 95% confidence interval = 4.82 to 8.55 cells per field, P<.001). No enrichment in the CD44+/CD24– or CD133+ population was detected in MCF-7/MDR. Conclusion: The cell population with cancer stem cell characteristics increased after prolonged continuous selection for doxorubicin resistance. PARALLEL study design with 4 samples Parental MCF-7 cell line versus Doxorubicin Resistant MCF-7 cell sublines Biological replicates: 2 parental controls, 2 drug resistant, independently grown and harvested. agent:Selection agent is multi-step doxorubicin selection: MCF7226ng, MCF7262ng biological replicate: MCF71, MCF72 biological replicate: MCF226ng, MCF7262ng
2011-09-25 | E-GEOD-24460 | biostudies-arrayexpress
Project description:Background: Cancer stem cells are presumed to have virtually unlimited proliferative and self-renewal abilities and to be highly resistant to chemotherapy, a feature that is associated with overexpression of ATP-binding cassette transporters. We investigated whether prolonged continuous selection of cells for drug resistance enriches cultures for cancer stem-like cells. Methods: Cancer stem cells were defined as CD44+/CD24– cells that could self-renew (ie, generate cells with the tumorigenic CD44+/CD24– phenotype), differentiate, invade, and form tumors in vivo. We used doxorubicin-selected MCF-7/ADR cells, weakly tumorigenic parental MCF-7 cells, and MCF-7/MDR, an MCF-7 subline with forced expression of ABCB1 protein. Cells were examined for cell surface markers and side-population fractions by microarray and flow cytometry, with in vitro invasion assays, and for ability to form mammospheres. Xenograft tumors were generated in mice to examine tumorigenicity (n = 52). The mRNA expression of multidrug resistance genes was examined in putative cancer stem cells and pathway analysis of statistically significantly differentially expressed genes was performed. All statistical tests were two-sided. Results: Pathway analysis showed that MCF-7/ADR cells express mRNAs from ABCB1 and other genes also found in breast cancer stem cells (eg, CD44, TGFB1, and SNAI1). MCF-7/ADR cells were highly invasive, formed mammospheres, and were tumorigenic in mice. In contrast to parental MCF-7 cells, more than 30% of MCF-7/ADR cells had a CD44+/CD24– phenotype, could self-renew, and differentiate (ie, produce CD44+/CD24– and CD44+/CD24+ cells), and overexpressed various multidrug resistance-linked genes (including ABCB1, CCNE1, and MMP9). MCF-7/ADR cells were statistically significantly more invasive in Matrigel than parental MCF-7 cells (MCF-7 cells = 0.82 cell per field and MCF-7/ADR = 7.51 cells per field, difference = 6.69 cells per field, 95% confidence interval = 4.82 to 8.55 cells per field, P<.001). No enrichment in the CD44+/CD24– or CD133+ population was detected in MCF-7/MDR. Conclusion: The cell population with cancer stem cell characteristics increased after prolonged continuous selection for doxorubicin resistance.
2011-09-26 | GSE24460 | GEO
Project description:Being the most malignant disease among females, breast cancer has morbidity and mortality in the first and second positions among various cancers [1]. Up to now, chemotherapy has been the most common therapy [2]; however, multidrug resistance (MDR) often occurs to give low overall survival rate. Thus, it is urgent to figure out the mechanism of chemotherapy resistance. The first step of drugs to attack tumor cells is to interact with the plasma membrane, and solute carrier (SLC) family proteins are uptake transporters [3]. On the other side, the efflux transporters (such as ATP-binding cassette, ABC) pump drug out of cancer cells [4]. The main mechanism of MDR is the upregulation of ATP-binding cassette (ABC) transporters [5]. Breast cancer resistance protein (ABCG2), multidrug resistance protein (ABCC1) and P-glycoprotein (P-gp) have been extensively studied [6,7]. Formation of CSCs [8], DNA damage [9] and cell apoptosis [10] and epithelial mesenchymal transition (EMT) are other mechanisms of MDR. To zoom in on the correlation between altered glycosylation and drug resistance and to find out the putative biomarkers, MS-based glycoprotomics is a method of choice. Here, we report our N-glycoproteomics study of differential N-glycosylation from the whole cell lysate of MCF-7/ADR CSCs (adriamycin-resistant MCF-7 CSCs) relative to MCF-7 CSCs. Intact N-glycopeptides from both cells were enriched with ZIC-HILIC, isotopically diethylated, mixed with 1:1 ratio, and the mixture was analyzed by C18-RPLC-ESI-MS/MS (HCD with stepped NCE). Differentially expressed N-glycopeptides (DEGPs) were identified and quantified with database search using GPSeeker.
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Project description:Currently, drug resistance of anti-cancer therapy has become the main cause of low survival rate and poor prognosis. Full understanding of drug resistance mechanisms is an urgent request for further development of anti-cancer therapy and improvement of prognosis. Here we present our N-glycoproteomics study of putative N-glycoprotein biomarkers of drug resistance in doxorubicin resistance breast cancer cell line michigan cancer foundation-7 (MCF-7/ADR) relative to parental michigan cancer foundation-7 (MCF-7) cells. Intact N-glycopeptides (IDs) from MCF-7/ADR and MCF-7 cells were enriched with zwitterionic hydrophilic interaction liquid chromatography (ZIC-HILIC), labeled with stable isotopic diethylation (SIDE), and analyzed with C18-RPLC-MS/MS (HCD with stepped normalized collision energies); these IDs were identifed with database search engine GPSeeker, and the diferentially expressed intact N-glycopeptides (DEGPs) were quantifed with GPSeekerQuan. With target-decoy searches and control of spectrum-level FDR≤1%, 322 intact N-glycopeptides were identifed; these intact N-glycopeptides come from the combination of 249 unique peptide backbones (corresponding to 234 intact N-glycoproteins) and 90 monosaccharide compositions (corresponding to 248 putative N-glycosites). The sequence structures of 165 IDs were confrmed with structure-diagnostic fragment ions. With the criteria of observation at least twice among the three technical replicates,≥1.5-fold change and p value<0.05, 20 DEGPs were quantifed, where fve of them were up-regulated and 15 of them were down-regulated; the corresponding intact N-glycoproteins as putative markers of drug resistance were discussed.
2023-12-30 | PXD036101 | Pride
Project description:N6-Methyladenosine (m6A) is the most abundant post-transcriptional modification in eukaryotes, the imbalance of which is reported to be associated with various pathological processes, including drug resistance. In this study, we analyzed the methylated RNA immunoprecipitation combined with next-generation sequencing (MeRIP-seq) data of AML cell line HL60 and its adriamycin-resistant cell line HL60/ADR. We found a total of 40550 peaks, representing 15640 genes in HL60, and a total of 38834 peaks, representing 15285 genes in HL60/ADR. A total of 4437 differentially methylated m6A peaks within 3461 genes have been found between HL60 and HL60/ADR. Among them, 3587 differentially m6A peaks within 2790 genes were hyper-methylated, and 850 m6A peaks within 671 genes were hypo-methylated. KEGG pathway analysis showed that pathways were enriched in tumor and drug-resistant related signaling pathway. Results of MeRIP-seq showed that fold enrichment of global m6A peaks was higher in HL60/ADR compared to HL60. This study provides a framework for the application of comprehensive mRNA m6A profiling towards acute myeloid leukemia cell line (HL60) and its adriamycin-resistant acute myeloid leukemia cell line (HL60/ADR).
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