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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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE93942 | GEO | 2018/03/01

REPOSITORIES: GEO

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Project description:In sub-Saharan Africa, endemic Kaposi’s sarcoma (EnKS) is still prevalent despite high incidence of epidemic Kaposi’s sarcoma (EpKS) resulting from the on-going HIV-1 epidemic. While KSHV is clearly the etiologic agent of KS, the mechanisms underlying KS development are not fully understood. For example, HIV-1 co-infection and concomitant immune dysfunction have been associated with EpKS development. However, the direct or indirect role(s) of HIV-1, and therefore of immune suppression, in EpKS remains unclear. How, or whether, EpKS is mechanistically distinct from EnKS is unknown. Thus, the absence of HIV-1 co-infection in EnKS provides a unique control for investigating and deciphering whether HIV-1 plays a direct or indirect role in the EpKS tumor microenvironment. We hypothesized that HIV-1 co-infection would induce transcriptome changes that differentiate EpKS from EnKS, thereby defining the direct intra-tumor role of HIV-1 in KS. Comparison of ART-treated and -naïve patients would further define the impact of ART on the KS transcriptome. We utilized RNA-seq followed by multiparameter bioinformatics analysis to compare transcriptomes from KS lesions to uninvolved control skin. We provide the first transcriptomic comparison of EpKS versus EnKS, ART-treated vs. –naïve EpKS and male vs. female EpKS to define the roles of HIV-1 co-infection, the impact of ART, and gender on KS gene expression profiles. Our findings suggest that ART-use and gender have minimal impact on transcriptome profiles of KS lesions. Gene expression profiles strongly correlated between EpKS and EnKS patients (Spearman r=0.83, p<10-10). A subset of genes involved in tumorigenesis and inflammation/immune responses showed higher magnitude, but not unique dysregulation in EnKS compared to EpKS. While gender and ART had no detectable contribution, the trend toward higher magnitude of gene dysregulation in EnKS coupled with the absence of HIV-1 transcripts in EpKS may suggest an indirect or systemic effect of HIV-1 to promote KS tumorigenesis.

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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

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