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Artesunate overcomes the resistance of basal type of bladder cancer to RC48

ABSTRACT: Artesunate overcomes the resistance of basal type of bladder cancer to RC48

PROVIDER: PRJNA996609 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25339972_1.fastq.gz	Fastqsanger.gz
	SRR25339972_2.fastq.gz	Fastqsanger.gz
	SRR25339973_1.fastq.gz	Fastqsanger.gz
	SRR25339973_2.fastq.gz	Fastqsanger.gz
	SRR25339974_1.fastq.gz	Fastqsanger.gz

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Artesunate overcomes the resistance of basal type of bladder cancer to RC48

Project description:ERBB2 expression mediates sensitivity of bladder cancer cells to RC48. JAK/STAT3 pathways compensatory activation after exposing RC48. A combination of STAT3 inhibitor-artesunate and RC48 could significantly inhibit basal bladder cancer growth. These findings provided a theoretical foundation for subsequent individualized therapy for MIBC based on the molecular types.

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Differential Gene expression anslysis between artesunate sensitive and resistat Leishmania donovani

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Rosiglitazone and Trametinib to treat basal bladder tumors

Project description:Rosiglitazone and Trametinib to treat basal bladder tumors

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Exploring the molecular mechanism of artesunate intervening in glioma based on DNA methylation sequencing technology

Project description:Whole gene methylation profiles of U87 and U251 glioma cells before and after artesunate treatment, Infinium MethylationEPIC BeadChip, samples including 3 U87 cell normal group, 3 U251 cell normal group, 3 artesunate treated U87 cell group, U251 cell group was treated with 3 artesunate.

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Project description:In vitro and in vivo studies including single cell sequencing showed that LPAR6 and CAB39L play a major role in regulating basal to luminal urothelial differentiation. Their loss of function contributed to bladder carcinogenesis by dysregulating urothelial differentiation program and sensitizing the urothelium to N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) induced cancers, which recapitulated luminal and basal subtypes of human bladder cancer.

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Transcription profiling of Plasmodium falciparum synchronized blood stages exposed to lethal doses of artesunate

Project description:Each experiment consisted in an artesunate-free culture (control) and an artesunate treated culture. For each time point explored, cDNA from parasites with and without the drug were labeled with different cyanines, mixed and hybridized. To analyse dynamic transcriptome alterations, two pilot experiments were performed in which RNA was harvested at 90 and 180 minutes of incubation with the drug. <br><br> Since artesunate is active on ring stages as well as on older trophozoite stages, we decided to explore different time points along the erythrocytic cycle and search for genes affected at each time point. Therefore, five drug treatment experiments, staggered between 20 hours and 30 hours of parasite development, were performed for the comparison of drug versus no drug at 90 minutes and 3 hours. <br><br> Different expression levels in artesunate-exposed vs. control unexposed cultures could reflect the added effects of the actual response to artesunate together with a possible difference in growth rate/developmental stage. To identify the developmentally regulated genes in the artesunate-free control culture, the 3 hours RNA was hybridized against the time 0 RNA (3 control experiments).

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Artesunate inhibits the cell viability of diffuse large B cell lymphoma cells by increasing the susceptibility to ferroptosis (RNA-seq).

Project description:Comparing the effects of artesunate versus DMSO in three DLBCL cell lines, we found a decrease in cell viability to 80%-60%. Over increasing artesunate dosage,we found increasing ROS generation and lipid peroxidation. In combination with the Ferrostatin-1 rescue experiment, we conclude that cell death induced by artesunate is ferroptotic. We compared the transcriptome of the U2932 cell line with and without 100µm artesunate in triplicate. A ferroptosis gene signature is shown to be enriched among the upregulated genes of this comparison. GPX4 protein expression was shown to be downregulated after artesunate in U2932 cells, but not in the rescue experiment with Ferrostatin-1. MT1G gene expression was identified as required for artesunate-mediated ferroptosis via targeted suppression by shRNAs. We present significantly decreased cell viability when combining artesunate with doxorubicin, suggesting a potential translation into clinic for treatment of ABC and GCB DLBCL.

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