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Whole-transcriptomic Profile of SK-MEL-3 Melanoma Cells Treated with the Histone Deacetylase Inhibitor: Trichostatin A.
Cancer Genomics & Proteomics ( IF 2.6 ) Pub Date : 2018-9-9 , DOI: 10.21873/cgp.20094
Elizabeth A Mazzio 1 , Karam F A Soliman 1
Affiliation  

Malignant melanoma cells can rapidly acquire phenotypic properties making them resistant to radiation and mainline chemotherapies such as decarbonize or kinase inhibitors that target RAS-proto-oncogene independent auto-activated mitogen-activated protein kinases (MAPK)/through dual specificity mitogen-activated protein kinase (MEK). Both drug resistance and inherent transition from melanocytic nevi to malignant melanoma involve the overexpression of histone deacetylases (HDACs) and a B-Raf proto-oncogene (BRAF) mutation.

中文翻译:

用组蛋白去乙酰化酶抑制剂:曲古抑菌素A处理的SK-MEL-3黑色素瘤细胞的完整转录组谱。

恶性黑色素瘤细胞可快速获得表型特性,使其对放射线和主线化学疗法具有抵抗力,例如脱碳或靶向RAS原癌基因独立的自动激活的促丝裂原激活的蛋白激酶(MAPK)的激酶抑制剂/通过双重特异性促分裂原激活的蛋白激酶(MEK)。耐药性和从黑素细胞痣向恶性黑色素瘤的固有转变都涉及组蛋白脱乙酰基酶(HDAC)的过表达和B-Raf原癌基因(BRAF)突变。
更新日期:2020-08-21
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