ScRNAseq of BRAF-mutant Colo205 cells control or treated for 24h or 72h with vemurafenib
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB41852 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4972711_1.fastq.gz | Fastqsanger.gz | |||
| ERR4972711_2.fastq.gz | Fastqsanger.gz | |||
| ERR4972712_1.fastq.gz | Fastqsanger.gz | |||
| ERR4972712_2.fastq.gz | Fastqsanger.gz | |||
| ERR4972713_1.fastq.gz | Fastqsanger.gz |
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Project description:The experiment investigates transcriptional response of BRAF-mut Colo205 cancer cells following treatment for 24h or 72h with BRAF-inhibitor vemurafenib compared to control cells on a single cell level.
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Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of RNAs in BRAFV600E+ thyroid cancer cell lines 8505C and WRO. We generated genome-wide transcriptome maps of 8505C and WRO cells after vemurafenib, BRAF inhibitor, treatment. In addition, we generated genome-wide transcriptome maps of clonally selected vemurafenib-resistant 8505C and WRO cells with or without vemurafenib treatment. Negative control treatment was 0.1% of dimethy solfoxide (DMSO), the diluent used to resuspend vemurafenib. The treatment regine of vemurafenib was 2 µM concentration for 24 hours. We find that both inducible response to BRAFi and acquired BRAFi resistance in thyroid cancer cells showed significant activation of the JAK/STAT pathway. Our study demonstrates that the JAK/STAT-signaling pathway is activated as thyroid cancer cells develop resistance to BRAFi and that this pathway is a potential target for anticancer activity and to overcome drug resistance that commonly develops to treatment with BRAFi in thyroid cancer and potentially in other malignancies.
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Project description:BRAF targeted drug vemurafenib have shown very good clinical benefit in melanoma patient containing BRAF V600E mutation. However, resistance always occurs in patient. Early stage of the resistance development require the tumor cell adapted to the targeted drug. We are trying to study the kinetic of melanoma cell adaptation towards vemurafenib. 10 melanoma cell lines with BRAF mutation are treated with targeted therapy vemurafenib. RNA-seq samples are collected after drug treatment for different time (day3 and day21) to compare with DMSO-treated control samples for each cell line. Except innate resistant cell line M381, all other cell lines shows inhibition of proliferation. However, a small cluster of cell lines (M397, M229 and M263) shows some other unique transcriptomic change. For cell line M397, M229 and M263, we also collected the RNA-seq data for long-term (73day/90day) drug treatment condition where the cells developed resistance to vemurafenib treatment. Dedifferentiation is enriched in these unique transcriptomic change within these 3 cell lines. Similar cell state dedifferentiation phenomenon is also reported to cause resistance towards immunotherpay where the resistant de-differentiated melanoma cells are induced by TNF which is secreted by tumor-infiltrating T cells. We also treat our cultured melanoma cells with TNF and collected the treated sample for RNA-seq experiment.
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