Division of Molecular Medicine, Ruđer Bošković Institute, Bijenička 54, HR-10000 Zagreb, Croatia.
Invest New Drugs. 2012 Apr;30(2):450-67. doi: 10.1007/s10637-010-9571-7. Epub 2010 Nov 3.
Six recently synthesized cyano-substituted heteroaryles, which do not bind to DNA but are highly cytotoxic against the human tumor cell line HeLa, were analyzed for their antitumor mechanisms of action (MOA). They did not interfere with the expression of human papillomavirus oncogenes integrated in the HeLa cell genome, but they did induce strong G1 arrest and result in the activation of caspase-3 and apoptosis. A computational analysis was performed that compared the antiproliferative activities of our compounds in 13 different tumor cell lines with those of compounds listed in the National Cancer Institute database. The results indicate that interference with cytoskeletal function and inhibition of mitosis are the likely antitumor MOA. Furthermore, a second in silico investigation revealed that the tumor cells that are sensitive to the cyano-substituted compounds show differences in their expression of locomotion genes compared with that of insensitive cell lines, thus corroborating the involvement of the cytoskeleton. This MOA was also confirmed experimentally: the cyano-substituted heteroaryles disrupted the actin and the tubulin networks in HeLa cells and inhibited cellular migration. However, further analysis indicated that multiple MOA may exist that depend on the position of the cyano-group; while cyano-substituted naphthiophene reduced the expression of cytoskeletal proteins, cyano-substituted thieno-thiophene-carboxanilide inhibited the formation of cellular reactive oxygen species.
六种新合成的氰基取代杂芳族化合物,它们不与 DNA 结合,但对人肿瘤细胞系 HeLa 具有高度细胞毒性,被分析其抗肿瘤作用机制(MOA)。它们不干扰整合在 HeLa 细胞基因组中的人乳头瘤病毒致癌基因的表达,但它们确实诱导强烈的 G1 期阻滞,并导致 caspase-3 的激活和细胞凋亡。进行了计算分析,比较了我们的化合物在 13 种不同肿瘤细胞系中的增殖活性与国立癌症研究所数据库中列出的化合物的活性。结果表明,干扰细胞骨架功能和抑制有丝分裂可能是抗肿瘤的作用机制。此外,第二次计算机模拟研究表明,对氰基取代化合物敏感的肿瘤细胞与不敏感的细胞系相比,其运动基因的表达存在差异,从而证实了细胞骨架的参与。该作用机制也通过实验得到了证实:氰基取代的杂芳族化合物破坏了 HeLa 细胞中的肌动蛋白和微管网络,并抑制了细胞迁移。然而,进一步的分析表明,可能存在多种作用机制,这些机制取决于氰基的位置;虽然氰基取代的萘并噻吩降低了细胞骨架蛋白的表达,但氰基取代的噻吩并噻吩甲酰胺抑制了细胞活性氧的形成。