...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >CHML suppresses cell growth and induces apoptosis in multiple human tumor lines.
【24h】

CHML suppresses cell growth and induces apoptosis in multiple human tumor lines.

机译：CHML抑制细胞生长并诱导多种人类肿瘤细胞凋亡。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

In the present study, we have investigated the effect of cytotropic heterogeneous molecular lipid (CHML), a new anticancer agent, on growth suppression in a variety of human tumor cell lines. At a non-toxic concentration (a range from 25 micrograms/ml to 100 micrograms/ml), CHML has shown to strongly inhibit tumor cell growth by using a typical colony survival assay. At a treatment of concentration of 50 micrograms/ml for 6 hours, CHML is able to suppress 50% of the tumor cell colony formation. At a concentration of 100 micrograms/ml (the therapeutic dosage in the clinical trial), more than 90% of the cells were killed in human breast carcinoma MCF-7, colorectal carcinoma RKO, kidney carcinoma G410, lung carcinoma and human myeloid leukemia ML-1 lines. In contrast, growth suppression of non-cancerous human skin fibroblasts by CHML was observed much less than that seen in tumor lines. These results indicate that CHML is an efficient inhibiting agent in tumor cell growth and is able to generate greater suppression in tumor cells than in noncancerous cells. With the use of DNA fragmentation assay, CHML was found to induce apoptosis in MCF-7, ML-1, H1299 and RKO lines after treatment at a concentration of 75 micrograms/ml for 8 hours. Following the CHML treatment, the tumor suppressor p53 protein elevated in RKO cells at 2 h posttreatment. The induction of p53 reached a peak at 4 hr and returned to normal level 16 hr later. Consistent with this result, Bax, which is regulated by p53 and is able to promote apoptosis, was also found to increase in a same kinetic manner as p53. These results suggest that the p53-pathway is activated by CHML and the activation of p53 may contribute to CHML-induced apoptosis in some tumor cells, such as MCF-7, RKO and ML-1. Considering that CHML is able to induce apoptosis in H1299 cells, which are of p53-negative status, it is speculated that CHML induces programmed cell death through both the p53-dependent and- independent pathways.
机译：在本研究中，我们已经研究了一种新型的抗癌药，胞质异质分子脂质（CHML）对多种人类肿瘤细胞系中生长抑制的影响。在无毒浓度（25微克/毫升至100微克/毫升的范围内）下，CHML已显示通过使用典型的菌落存活分析法强烈抑制肿瘤细胞的生长。以50微克/毫升的浓度处理6小时后，CHML能够抑制50％的肿瘤细胞集落形成。在浓度为100微克/毫升（临床试验中的治疗剂量）下，超过90％的细胞在人乳腺癌MCF-7，大肠癌RKO，肾癌G410，肺癌和人髓样白血病ML中被杀死-1行。相反，观察到CHML对非癌性人皮肤成纤维细胞的生长抑制作用远小于在肿瘤系中观察到的生长抑制作用。这些结果表明，CHML是肿瘤细胞生长中的有效抑制剂，并且在肿瘤细胞中比在非癌细胞中能够产生更大的抑制作用。使用DNA片段测定法，发现CHML可以在以75微克/毫升的浓度处理8小时后诱导MCF-7，ML-1，H1299和RKO系发生凋亡。 CHML处理后，RKO细胞中的肿瘤抑制p53蛋白在处理后2小时升高。 p53的诱导在4小时达到峰值，并在16小时后恢复到正常水平。与该结果一致，还发现由p53调节并能够促进细胞凋亡的Bax以与p53相同的动力学方式增加。这些结果表明p53途径被CHML激活，并且p53的激活可能有助于CHML诱导的某些肿瘤细胞如MCF-7，RKO和ML-1的凋亡。考虑到CHML能够诱导处于p53阴性状态的H1299细胞凋亡，因此推测CHML通过p53依赖性和非依赖性途径诱导程序性细胞死亡。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号