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Drug-resistant breast cancer stem cells enriched through one-dose chemo-therapy convey drug tolerance.

ABSTRACT: Drug-resistant breast cancer stem cells enriched through one-dose chemo-therapy convey drug tolerance.

PROVIDER: PRJEB40472 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4615350.fastq.gz	Fastqsanger.gz
	ERR4615351.fastq.gz	Fastqsanger.gz
	ERR4615352.fastq.gz	Fastqsanger.gz
	ERR4615353.fastq.gz	Fastqsanger.gz
	ERR4615354.fastq.gz	Fastqsanger.gz

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Drug-resistant breast cancer stem cells enriched through one-dose chemo-therapy convey drug tolerance.

Project description:The murine basal-like mammary carcinoma cell line H8N8 was transplanted into syngeneic WAP-T mice and growing tumors were subjected to a single dose of combination chemotherapy (100 mg/kg body weight cyclophosphamide, 5 mg/kg BW doxorubicin and 100 mg/kg BW 5-FU, short CAF). Mice of the control group were treated with one injection vehicle solution. Three cohorts of animals were generated: control, remission, and regrowth group. Tumor cells were isolated from lesions of each group, purified by flow cytometry to remove non-tumor cells and debris, and finally subjected to whole transcriptome analysis by mRNA-sequencing.

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Project description:Measuring dose-dependent effects of drugs on post-translational modifications on a proteome-wide scale reveals how these drugs work in cells. Here, we present a quantitative chemical proteomic approach termed decryptM, able to assess target and pathway engagement as well as the mode of action (MoA) of diverse cancer drugs in cells by measuring their dose- (and time-) resolved modulation of PTMs on a proteomic scale. Data collected for 31 drugs, representing six drug classes in 13 human cell lines, demonstrate that the approach is widely applicable. The body of data represents ~1.8 million quantitative cellular drug assays (dose-response curves) including 47502 regulated p-peptides (of 124660 detected on 11982 proteins), 7316 Ubi-peptides (of 9173 detected on 3006 proteins), and 546 Ac-peptides (of 2478 detected on 1377 proteins). Most PTMs were not regulated by most drugs, which is highly valuable information for understanding which pathways are addressed (or not) by each drug in cells. The decryptM data have been incorporated into ProteomicsDB and can be explored interactively. The raw files, searches, curves files, and result PDFs can be downloaded here. For details, have a look at the Experiment_summary.xlsx.Paper: doi/10.1126/science.ade3925

2023-03-17 | PXD037285 | Pride

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MCF7 dose response

Project description:ErbB receptor ligands, epidermal growth factor (EGF) and heregulin (HRG), induce dose-dependent transient and sustained intracellular signaling, proliferation and differentiation of MCF-7 breast cancer cells, respectively. In an effort to delineate the ligand-specific cell determination mechanism, we investigated time-course gene expressions induced by EGF and HRG that induce distinct cellular phenotypes in MCF-7 cells. To analyze the effects of ligand dosage and time for the gene expression independently, we developed a statistical method for decomposing the expression profiles into the two effects. Our results indicated that signal transduction pathways devotedly convey quantitative properties of the dose-dependent activation of ErbB receptor to early transcription. The results also implied that moderate changes in the expression levels of numbers of genes, not the predominant regulation of a few specific genes, might cooperatively work at the early stage of the transcription for determining the cell fate. However, the EGF- and HRG-induced distinct signal durations resulted in the ligand-oriented biphasic induction of proteins after 20 min. The selected gene list and HRG-induced prolonged signaling suggested that transcriptional feedback to the intracellular signaling results in a graded to biphasic response in the cell determination process, and that each ErbB receptor is inextricably responsible for the control of amplitude and duration of cellular biochemical reactions. Keywords: time course, dose response

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