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首页> 外文期刊>Cell cycle >Novel anticancer compounds induce apoptosis in melanoma cells.
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Novel anticancer compounds induce apoptosis in melanoma cells.

机译：新型抗癌化合物诱导黑素瘤细胞凋亡。

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摘要

We previously described the identification of a nucleoside analog transcriptional inhibitor ARC (4-amino-6-hydrazino-7-beta-D-ribofuranosyl-7H-Pyrrolo[2,3-d]-pyrimidine-5-carbox amide) and FoxM1 inhibitor, thiazole antibiotic Siomycin A that were able to induce apoptosis in cancer cell lines of different origin. Here, we report the characterization of these drugs on a panel of melanoma cell lines. We found that in contrast to the common anti-melanoma drug dacarbazine (DTIC), ARC and thiazole antibiotics, Siomycin A and thiostrepton, efficiently inhibited growth and induced cell death in melanoma cell lines in low concentrations. Overexpression of the antiapoptotic protein Mcl-1 protected melanoma cells from apoptosis induced by these compounds. Furthermore, we found that ARC and Siomycin A synergistically induce apoptosis in DM833 melanoma cell line suggesting that they may antagonize different anti-apoptotic pathways in melanoma cells. In general, these drugs may represent important candidates for anti-cancer drug development against melanoma.
机译：我们以前描述了核苷类似物转录抑制剂ARC（4-氨基-6-肼基-7-β-D-呋喃呋喃糖基-7H-吡咯并[2,3-d]-嘧啶-5-羧酰胺）和FoxM1抑制剂的鉴定噻唑抗生素Siomycin A，能够诱导不同来源的癌细胞系发生凋亡。在这里，我们在一组黑色素瘤细胞系上报告了这些药物的表征。我们发现，与常见的抗黑素瘤药物达卡巴嗪（DTIC），ARC和噻唑抗生素，Siomycin A和thiostrepton相比，低浓度的黑素瘤细胞系可有效抑制其生长并诱导细胞死亡。抗凋亡蛋白Mcl-1的过表达保护黑素瘤细胞免受这些化合物诱导的凋亡。此外，我们发现ARC和Siomycin A协同诱导DM833黑色素瘤细胞系中的细胞凋亡，表明它们可能拮抗黑色素瘤细胞中不同的抗凋亡途径。通常，这些药物可能代表了针对黑色素瘤的抗癌药物开发的重要候选药物。

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