Suppr超能文献

过氧化氢酶保护肿瘤细胞免受细胞间 ROS 信号诱导的细胞凋亡。

Catalase protects tumor cells from apoptosis induction by intercellular ROS signaling.

机构信息

Harvard Medical School, BIDMC, Departmentof Matrix Biology, Boston, MA 02215, USA.

出版信息

Anticancer Res. 2009 Nov;29(11):4541-57.

Abstract

Transformed cells are subject to intercellular induction of apoptosis by neighbouring nontransformed cells and to autocrine apoptotic self-destruction. Both processes depend on extracellular superoxide anion generation by the transformed cells and on the release of peroxidase from both nontransformed and transformed cells. This concerted action results in HOCl synthesis, HOCl-superoxide anion interaction and generation of apoptosis-inducing hydroxyl radicals. In contrast to transformed cells, ex vivo tumor cells are resistant against intercellular induction of apoptosis and autocrine apoptotic self-destruction. Resistance of tumor cells against intercellular ROS signaling depends on interference through catalase expression on the membrane. Intercellular ROS signaling of tumor cells can be restored when i) exogenous HOCl is added; ii) exogenous hydrogen peroxide is supplied, or iii) catalase is inhibited. These findings define the biochemical basis for specific apoptosis induction in tumor cells through re-establishment of intercellular ROS signaling, a potential novel approach in tumor prevention and therapy.

摘要

转化细胞易受相邻正常细胞诱导凋亡,也易发生自身凋亡。这两个过程都依赖于转化细胞产生细胞外超氧阴离子和正常细胞及转化细胞释放过氧化物酶。这种协同作用导致次氯酸(HOCl)合成、HOCl-超氧阴离子相互作用以及诱导凋亡的羟自由基生成。与转化细胞相反,体外肿瘤细胞抵抗细胞间诱导凋亡和自身凋亡。肿瘤细胞对细胞间 ROS 信号的抵抗取决于通过膜上的过氧化氢酶表达进行干扰。当:i)加入外源性次氯酸;ii)提供外源性过氧化氢;或 iii)抑制过氧化氢酶时,肿瘤细胞的细胞间 ROS 信号可以被恢复。这些发现为通过重新建立细胞间 ROS 信号来特异性诱导肿瘤细胞凋亡定义了生化基础,这是肿瘤预防和治疗的一种潜在新方法。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验