Food Science & Nutrition, 2016.

Genistein suppresses the proliferation of telomerase negative cells

Chuan Chuan Lin, Meng Hsun Hsieh, Shu Chun Teng

Department of Food Science, China University of Science and Technology, Taipei 115, Taiwan; Department of Microbiology, College of Medicine, National Taiwan University, Taipei 100, Taiwan

In both tumor and yeast cells that lack telomerase, telomeres are maintained via an alternative recombination mechanism. In this study, we tested genistein, a potential TOP2 inhibitor required for telomere–telomere recombination, on the repression of telomere–telomere recombination. Genistein on the repression of type II recombination on a tlc1 yeast strain was examined by the telomeric DNA structures using Southern blot analysis. Telomere patterns of freshly dissected tlc1 spores containing an empty plasmid (pYES2) or a yeast TOP2 (yTOP2) plasmid were analyzed. The results indicated that the reintroduction of TOP2 recovered the type II pattern, implying genistein in the blockage of type II survivors in the tlc1 strain. The effects of genistein on both tlc1 and tlc1 rad 51 strains in liquid and solid mediums were also examined. Finally, treatment of 10 μmol/L of genistein showed inhibitory effect on the growth of telomerase-negative U2OS alternative lengthening of telomere (ALT) cells, but not in telomerase-positive HCT116 cells. These results provide evidences that the inhibitory effects of genistein on telomerase-negative cells depend on type II recombination pathway in yeast and the ALT pathway in human tumors.

食品科学与营养，2016。

染料木黄酮抑制端粒酶阴性细胞的增殖

林川川，孟春松，滕树春

中国科学技术大学食品科学系，台北115，台湾; 台湾大学医学院微生物系，台北100，台湾

在缺乏端粒酶的肿瘤和酵母细胞中，端粒通过替代重组机制维持。在这项研究，我们测试染料木素，端粒端粒重组潜在的TOP2抑制剂，对端粒端粒重组的镇压。使用Southern印迹分析通过端粒DNA结构检测染料木黄酮对tlc1酵母菌株上II型重组抑​​制的抑制作用。分析含有空质粒（pYES2）或酵母TOP2（yTOP2）质粒的新鲜解剖的tlc1孢子的端粒模式。结果表明，TOP2的重新引入恢复了II型模式，意味着染料木黄酮在tlc1菌株中II型存活者的阻断中。还检查了染料木素对液体和固体培养基中tlc1和tlc1 rad 51菌株的作用。最后，处理10μmol/ L的染料木黄酮显示对端粒酶阴性U2OS替代延长端粒（ALT）细胞的生长的抑制作用，而不是在端粒酶阳性HCT116细胞中。这些结果提供证据，染料木黄酮对端粒酶阴性细胞的抑制作用依赖于酵母中的II型重组途径和人肿瘤中的ALT途径。