Expression data from BRAFV600E A375 melanoma cells treated with vehicle or vemurafenib

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.

维莫非尼（Vemurafenib）是一种BRAF抑制剂（BRAF inhibitor），对黑色素瘤中最常见的BRAF突变体（BRAFV600E）具有特异性。维莫非尼通过抑制MEK/ERK丝裂原活化蛋白激酶的下游激活，抑制BRAF突变型人黑色素瘤细胞的增殖。本研究使用基因芯片（microarrays）检测维莫非尼敏感型BRAFV600E人黑色素瘤细胞系（A375）对维莫非尼的转录应答，以进一步阐明BRAFV600E驱动人黑色素瘤细胞增殖与能量代谢的分子机制。将BRAFV600E型A375人黑色素瘤细胞用溶剂对照（0.1%二甲基亚砜，DMSO）或10 μM维莫非尼处理24小时，随后提取总RNA。实验分为3个独立批次完成（分别于3天内使用3批不同的细胞储备液制备样本并提取RNA），共获得3次独立生物学重复（n=3）。于同一天使用同一批细胞储备液制备的配对重复样本，分别以A、B、C标注。