Molecular mechanisms of prostate cancer cell death triggered by inhibition of arachidonate 5-lipoxygenase: involvement of Fas death receptor-mediated signals.
Molecular mechanisms of prostate cancer cell death triggered by inhibition of arachidonate 5-lipoxygenase: involvement of Fas death receptor-mediated signals.
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花生四烯酸 5-脂氧合酶抑制引发的前列腺癌细胞死亡的分子机制：Fas 死亡受体介导信号的参与。
DOI：
10.1007/978-1-4615-0193-0_64
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发表时间：
2002
影响因子：
--
通讯作者：
Myers,CharlesE
中科院分区：
文献类型：
--
作者：
Ghosh,Jagadananda;Myers,CharlesE
癌症是细胞不受控制的增殖的结果，已经成为世界上最常见的人类健康挑战之一。虽然新细胞的形成是癌症生物学中不可或缺的一部分，但近年来，肿瘤细胞的减少死亡已成为人们关注的焦点，因为它是导致组织动态平衡失调导致癌症相关肿瘤负担的主要原因。细胞损失系数是肿瘤生长速度的主要决定因素，在某些情况下，其值高达90%(1)。化疗药物旨在通过阻止细胞分裂和/或增加细胞死亡来逆转癌细胞的行为顺序。细胞凋亡，或程序性细胞死亡，是一种通过进化年龄保存下来的基于基因的自杀机制，通过这种机制，感染和受损的细胞以受控的方式选择性地从体内清除，而不会产生太多的炎症或旁观者效应。它是多细胞物种中细胞死亡的主要机制。目前用于癌症化疗的药物，在大多数情况下，通过膜定位的细胞死亡受体介导的信号或线粒体的参与，通过诱导细胞凋亡来发挥作用。包括放射治疗、免疫治疗和激素消融在内的其他癌症治疗方法也通过细胞凋亡来诱导细胞死亡。另一方面，肿瘤细胞通过解除对细胞死亡程序(药物新耐药)的调控，或通过在其表面表达细胞死亡信号诱导配体来反击抗肿瘤淋巴细胞来产生免疫耐药，从而构成耐药威胁。
Cancer is the result of uncontrolled cell proliferation and has emerged as one of the most frequently diagnosed challenges to human health all over the world. While formation of new cells is an integral part of cancer biology, decreased death of tumor cells has recently emerged as a focus of attention as the leading cause of deregulated tissue homeostasis resulting in cancer-related tumor burden. The cell loss factor is the major determinant of tumor growth rate with values approaching to as high as 90% in some case (1). Chemotherapeutic drugs are designed to reverse the order of cancer cell behavior by blocking cell division and/or increasing cell death. Apoptosis, or programmed cell death, is a genetically based suicide mechanism preserved through evolutionary ages (2), by which infected and damaged cells are selectively eliminated from the body in a controlled fashion without much inflammatory or bystander effects. It is the dominant mechanism of cell death in multicellular species. Drugs currently in use for cancer chemotherapy, in most cases, work by induction of apoptosis, either through membrane-localized cell death receptor-mediated signals or by the involvement of mitochondria. Other cancer-therapeutic modalities including radiotherapy, immunotherapy and hormone ablation also induce cell death by apoptosis. Tumor cells, on the other hand, are posing a threat of drug-resistance by deregulating the cell-death program (“drug neo-resistance”) or immuno-resistance by expressing cell death signal-inducing ligands on their surface to counterattack the antitumor lymphocytes.