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Transiently enhanced multi-drug resistance by epigenetic mechanism from reprogrammed cancer cell model

ABSTRACT: Transiently enhanced multi-drug resistance by epigenetic mechanism from reprogrammed cancer cell model

PROVIDER: PRJNA579059 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10333585.fastq.gz	Fastqsanger.gz
	SRR10333586.fastq.gz	Fastqsanger.gz
	SRR10333587.fastq.gz	Fastqsanger.gz
	SRR10333588.fastq.gz	Fastqsanger.gz
	SRR10333589.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transiently enhanced multi-drug resistance by epigenetic mechanism from reprogrammed cancer cell model

Project description:Background: Drug resistance by epigenetic modulation in cancer cells has been suggested, and the epigenetic-driven heterogeneity has been suggested as an important mechanism. To elucidate the epigenetic mechanism further, epigenetically reprogrammed cancer (R-cancer) cells were established and their resistance during differentiation was analyzed. Methods: R-cancer cells for H460 (R-H460) were established by transient introduction of reprogramming factors. Then, differentiated R-H460 (dR-H460) cells were prepared by withdrawal of stem cell media (SCM) for various durations, and the changes in drug resistance were tested. Results: dR-H460 cells with SCM-withdrawal for about 2 weeks (mdR-H460 cells) formed significantly more drug-resistant colonies to both cisplatin and paclitaxel. The resistant phenotype of the cisplatin resistant colonies from mdR-H460 cells, however, was lost after long-term (about 70-90 days) cisplatin-withdrawal, suggesting a transient epigenetic mechanism. In another R-cancer cell model with N87, the increased drug-resistance was also observed for both cisplatin and paclitaxel after SCM-withdrawal. In single cell analyses, heterogeneity did not increase significantly in mdR-H460, although relatively higher fraction of mdR-H460 cells was observed in several clusters of parent H460 cells. Conclusion: Based on R-cancer model, increased cancer cell population under epigenetic transition, rather than heterogeneity from epigenetic changes, may confer the epigenetic-driven drug resistance, which can provide a new strategy to fight cancers by control of cancer cells under epigenetic transition.

2020-10-22 | GSE139275 | GEO

Drug Discovery For Diamond Blackfan Anemia Using Reprogrammed Hematopoietic Progenitors

Project description:Diamond-Blackfan anemia (DBA) is a congenital disorder characterized by the failure of erythroid progenitor differentiation, severely curtailing red blood cell production. Because many DBA patients fail to respond to corticosteroid therapy, there is considerable need for therapeutics for this disorder. Identifying therapeutics for DBA requires circumventing the paucity of primary patient blood stem and progenitor cells. To this end, we adopted a reprogramming strategy to generate expandable hematopoietic progenitor cells from induced pluripotent stem cells (iPSCs) from DBA patients. Reprogrammed DBA progenitors recapitulate defects in erythroid differentiation which were rescued by gene complementation. Unbiased chemical screens identified SMER28, a small molecule inducer of autophagy, which enhanced erythropoiesis in a range of in vitro and in vivo models of DBA. SMER28 acted through autophagy factor ATG5 to stimulate erythropoiesis and upregulate expression of globin genes. These findings present an unbiased drug screen for hematological disease using iPSCs and identify autophagy as a therapeutic pathway in DBA.

2017-01-01 | GSE90940 | GEO

Directly Reprogrammed Human Neurons Identify a Pathogenic Mechanism of Valproic Acid at Early Developmental Stages

Project description:Human pluripotent stem cells can be rapidly converted into functional neurons by ectopic expression of proneural transcription factors. Here we show that directly reprogrammed neurons, despite their rapid maturation kinetics, can model teratogenic mechanisms that specifically affect early neurodevelopment. We delineated distinct phases of in vitro maturation during reprogramming of human neurons and assessed the cellular phenotypes of valproic acid (VPA), a teratogenic drug. VPA exposure caused chronic impairment of dendritic morphology and functional properties of developing neurons, but not those of mature neurons. These pathogenic effects were associated with VPA-mediated inhibition of the histone deacetylase (HDAC) and glycogen synthase kinase-3 (GSK-3) pathways, which caused transcriptional downregulation of many genes, including MARCKSL1, an actin-stabilizing protein essential for dendritic morphogenesis and synapse maturation during early neurodevelopment. Our findings identify a developmentally restricted pathogenic mechanism of VPA and establish the use of reprogrammed neurons as an effective platform for modeling teratogenic pathways.

2019-05-28 | GSE129241 | GEO

Enhanced combination treatment on osteosarcoma by mitigating drug-induced oncogenic signaling pathway activation

Project description:Enhanced combination treatment on osteosarcoma by mitigating drug-induced oncogenic signaling pathway activation

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Alveolar Macrophages Maintain Tissue Localization and Gain Enhanced Anti-Tumor Activity in Lewis Lung Carcinoma-Reprogrammed Lung Microenvironment

Project description:Alveolar Macrophages Maintain Tissue Localization and Gain Enhanced Anti-Tumor Activity in Lewis Lung Carcinoma-Reprogrammed Lung Microenvironment

| PRJNA1287729 | ENA

Retrobiosynthesis of unnatural lactams via reprogrammed polyketide synthase

Project description:Using discovery global proteomics to study the retrobiosynthesis of unnatural lactams via reprogrammed polyketide synthase.

2025-01-28 | MSV000096981 | MassIVE

Reprogrammed alveolar macrophages after pneumonia recovery

Project description:Reprogrammed alveolar macrophages after pneumonia recovery

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RNA Sequencing for reprogrammed beta cells

Project description:RNA Sequencing for reprogrammed beta cells

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Complexity of expression from transiently transfected plasmids

Project description:Transient plasmid transfection is common approach for studies in cultured mammalian cells. To examine behavior of transfected plasmids, we analyzed their transcriptional landscape by deep sequencing. We found that plasmids generate different levels of transcripts virtually everywhere. Spurious transcription may have undesirable effects as some co-transfected plasmids inhibited expression of luciferase reporters in a dose-dependent manner. In one case, we attributed this effect to kan/neo resistance cassette, which generated a unique population of edited sense and antisense small RNAs. The unexpected complexity of expression of transiently transfected plasmids highlights the importance of appropriate experimental controls. HEK293 cells (human origin) transiently transfected with 4 various plasmids

2012-08-17 | E-GEOD-36062 | biostudies-arrayexpress

Global RNA expression of fibromodulin reprogrammed human BJ fibroblasts

Project description:RNA-seq analysis of fibromodulin reprogrammed human BJ fibroblasts to obtain the global transcripton of the yield fibromodulin reprogrammed (FReP) cells.

2019-08-10 | GSE104830 | GEO

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