Paired biopsies melanoma
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR445558.fastq.gz | Fastqsanger.gz | |||
| ERR445559.fastq.gz | Fastqsanger.gz | |||
| ERR445560.fastq.gz | Fastqsanger.gz | |||
| ERR445561.fastq.gz | Fastqsanger.gz | |||
| ERR445562.fastq.gz | Fastqsanger.gz |
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Project description:Vemurafenib is a BRAF inhibitor with specificity for the most common BRAF mutant encountered in melanomas (BRAFV600E). Vemurafenib suppresses the proliferation of BRAF mutant human melanoma cells by suppressing downstream activation of the MEK/ERK mitogen activated protein kinases. We used microarrays to examine the transcriptional response of a vemurafenib-sensitive BRAFV600E human melanoma cell line (A375) to vemurafenib in order to further delineate the mechanisms by which BRAFV600E drives cell proliferation and energy metabolism in human melanoma. BRAFV600E A375 human melanoma cells were treated with vehicle (0.1% DMSO) or 10 uM vemurafenib for 24 h after which total RNA was extracted. Cells were prepared and RNA was extracted in 3 separate batches (three different cell stocks on three separate days) providing three independent replicates (n=3). Paired replicates (prepared from the same stock of cells on the same day) are denoted by A, B and C.
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Project description:In order to identify mechanisms of melanoma treatment resistance, we applied micorofluidic scRNA-Seq to the transcripomes of a total of about 31,000 single cells obtained form A375 melanoma cell line untreated/sensitive or treated with BRAF inhibitor vemurafenib, either alone or in combination with MEK1 inihibitor cobimetinib or trametinib. Analysis by dimensionality reduction software tSNE and SOM identified a clonal heterogeneity clearly seperating all 4 possible treatment conditions.
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