ABSTRACT: Expression data for human chronic myeloid leukemia K562 cell line (KS) and adriamycin induced multidrug-resistant K562/ADR (KA) cell line before and after treatment with hypomethylating agent decitabine
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.
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.
Project description:Multidrug resistance (MDR) frequently develops in cancer patients exposed to chemotherapeutic agents and is usually brought about by over-expression of P-glycoprotein (P-gp) which acts as a drug efflux pump. MiRNAome profiling using next-generation sequencing identified differentially expressed microRNAs (miRs) between parental K562 cells and MDR K562 cells (K562/ADM) induced by chronic adriamycin treatment. MiRNAome profiling in untreated K562 cells and K562 cells exposed to long-term adriamycin treatment
Project description:A novel hypomethylating agent NTX-301 is a promising therapeutic agent for AML patients. To examine its mechanisms of action, we produced methylome data upon treatment with NTX-301 or decitabine (DAC) in MV4-11 cell line.
Project description:A novel hypomethylating agent NTX-301 is a promising therapeutic agent for AML patients. To examine its mechanisms of action, we produced gene expression data upon treatment with NTX-301 or decitabine (DAC) in MV4-11 cell line.
Project description:We compared the global RNA expression level between doxorubicin-sensitive human ovarian cancer cell line A2780 and the adriamycin-resistant cell line A2780-ADR to elucidate the drug resistant related molecular mechanisms or targets.
Project description:A novel hypomethylating agent NTX-301 is a promising therapeutic agent for AML patients. To examine its mechanisms of action, we produced gene expression data upon treatment with NTX-301 or decitabine (DAC) in AML cell lines.
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).
Project description:Cell lines representing human T-ALL were analyzed to compare GATA3low ETP-ALL (i.e. PER-117) with "typical" T-ALL. Moreover, changes in global gene expression were assessed comparing GATA3low ETP-ALL (i.e. PER-117) and GATA3high ETP-ALL (i.e. Loucy) upon treatment with Decitabine, a hypomethylating agent. Analysis of 6 human cell lines representing "typical" T-ALL (BE13, Jurkat, Molt4, RPM18402) and ETP-ALL (Loucy, PER-117). Additionally, global gene expression was assessed before and after treatment of ETP-ALL cell lines with Decitabine
Project description:To identify p53-regulated lncRNAs responsive to DNA damage in human hepatocellular carcinoma (HCC) cells, we conducted paired-end and strand-specific RNA-seq using HepG2 wild-type and p53-knockout (HepG2-KO-p53) cells, which were devoid of p53 protein, using the CRISPR-Cas9 system treated with or without the DNA-damaging agent adriamycin (ADR)
