Effect of nitric oxide on the reversal of adriamycin resistance in NCI/ADR-RES tumor cells
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PROVIDER: PRJNA561586 | ENA |
REPOSITORIES: ENA
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Project description:To understand how nitric oxide is involved in reversal of resistance and investigate mechanisms of Pgp-dependent efflux and genes in involved in drug resistance.
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Project description:Oncogene-induced senescence (OIS), a terminal cell cycle block countering (pre)neoplastic lesions, is characterised on the molecular level by trimethylated histone H3 lysine 9 (h3K9me3), a transcriptionally repressive chromatin mark linked to silencing of S-phase-promoting genes. Whether H3K9-governed chromatin remodelling influences anticancer treatment-induced senescence (TIS) and whether functional control of this mark impacts on treatment outcome is not known. We used global gene expression profiling by microarrays to gain insight into the molecular responses of Emu-myc; Suv39h1-/- B-cell lymphoma cells to senescence-inducing anticancer agent Adriamycin (ADR). Primary lymphoma cells isolated from lymph nodes of Emu-Myc; Suv39h1-/- mice were used. In this model, the c-Myc oncogene is constitutively expressed in the cells of the B-cell lineage, leading to spontaneous development of aggressive B-cell lymphomas. Adriamycin (ADR), a cytostatic drug used as a standard part of several lymphoma treatment regimens, is known to massively induce TIS in Suv39h1-proficient lymphomas, protected from apoptosis by Bcl-2 over expression (Myc;Bcl2). In order to discern the impact of Suv39h1 to TIS induction under these conditions, we analysed here transcriptional profiles of matched pairs of Emu-myc;Suv39h1-/-;Bcl2 lymphomas, untreated or treated for 5 days with ADR.
2013-07-04 | E-GEOD-44355 | biostudies-arrayexpress
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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Project description:To explore the mechanisim and signaling pathway of hypomethylating agent decitabine in reversing P-glycoprotein(P-gp) induced multidrug resistance, we used adriamycin to treat drug sensitive human chronic myeloid leukemia K562 cells(KS) and successfully induced multidrug-resistant K562/ADR (KA) cells that higher expression of drug efflux pump P-gp. Gene expression profile was used to analysis the difference gene expression before and after treated with decitabine in both KS and KA cells.
2018-03-01 | GSE93942 | GEO
Project description:Caenorhabditis elegans strain:N2, adr-1, adr-2, adr-1 adr-2 Transcriptome or Gene expression
| PRJNA82293 | ENA
Project description:The aim of this study was to compare the gene expression profile changes of DMBA-induced rat breast tumors after treatment with adriamycin. To this end, a cDNA microarray was performed (Affymetrix’s Rat Genome 230 2.0 array). This gene expression study was carried out on the tumor biopsy samples prior to adriamycin treatment, and compared with matched tumor biopsy samples after completion of the adriamycin treatment schedule. Breast tumors were induced with a single oral dosage of 7,12-dimethylbenz(alpha)anthracene (100 mg/kg body weight) in female Sprague-Dawley rats and subsequently treated with adriamycin (1 mg/kg body weight/week for 6 weeks) intravenously through lateral tail vein. Gene expression analysis was performed in paired samples as follows: ADR final trucut tumor vs initial trucut tumor (ADR final vs basal). For this assay, 5 samples were chosen according to histopathologic criteria (Bloom-Richardson grade II). Gene expression profiling was carried out using Affymetrix’s GeneChip technology, using the Rat Genome 230 2.0 array from this provider. All the protocols and apparatus were recommended by Affymetrix. Total RNA from frozen mammary tumors was extracted by RNeasy Mini kit and homogenized by QIAshredder columns according to manufacturer’s instructions. The quality and quantity of the obtained RNA was checked out through agarose electrophoresis and later spectrophotometry at 260/280 nm. Biotinylated cRNA was synthesized following the IVT labeling kit from Affymetrix and purified by the GeneChip Sample Cleanup Module from Affymetrix. The quality and quantity of the obtained cRNA was again checked out through agarose electrophoresis and posterior spectrophotometry at 260/280 nm. After hybridization, slides were washed and scanned following the manufacturer’s standard protocol. Intensity values were normalized by Robust Multichip Average method and subsequently these were filtered to remove the control sequences and those with a hybridization signal close to background. The spike controls were: BioB, BioC, BioD and Cre; because BioB was the least abundant in the samples, it was used to estimate the sensitivity of the experiment. The housekeeping control was GAPDH. After non-supervised clustering using Pearson correlation coefficient, statistical significance of gene expression was estimated by Student’s T test for paired samples, using GeneSpring GX 7.3 software (Agilent).
2009-06-01 | E-GEOD-16231 | biostudies-arrayexpress
Project description:Oncogene-induced senescence (OIS), a terminal cell cycle block countering (pre)neoplastic lesions, is characterised on the molecular level by trimethylated histone H3 lysine 9 (h3K9me3), a transcriptionally repressive chromatin mark linked to silencing of S-phase-promoting genes. Whether H3K9-governed chromatin remodelling influences anticancer treatment-induced senescence (TIS) and whether functional control of this mark impacts on treatment outcome is not known. We used global gene expression profiling by microarrays to gain insight into the molecular responses of Emu-myc; Suv39h1-/- B-cell lymphoma cells to senescence-inducing anticancer agent Adriamycin (ADR).
2013-07-04 | GSE44355 | GEO
Project description:Background:Ovarian cancer has the highest mortality rate among all the gynecological cancers. This is mostly due to the resistance of ovarian cancer to current chemotherapy regimens. Therefore, it is of crucial importance to identify the molecular mechanisms associated with chemoresistance. Methods:NCI/ADR-RES is a multidrug-resistant cell line that is a model for the study of drug resistance in ovarian cancer. We carried out a microarray-derived transcriptional profiling analysis of NCI/ADR-RES to identify differentially expressed genes relative to its parental OVCAR-8. Results:Gene-expression profiling has allowed the identification of genes and pathways that may be important for the development of drug resistance in ovarian cancer. The NCI/ADR-RES cell line has differential expression of genes involved in drug extrusion, inactivation, and efficacy, as well as genes involved in the architectural and functional reorganization of the extracellular matrix. These genes are controlled through different signaling pathways, including MAPK-Akt, Wnt, and Notch. Conclusion:Our findings highlight the importance of using orthogonal therapies that target completely independent pathways to overcome mechanisms of resistance to both classical chemotherapeutic agents and molecularly targeted drugs.
| S-EPMC5757493 | biostudies-literature