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三氧化二砷(As2O3)在血液系统肿瘤和多种实体肿瘤的治疗中已取得了一定的成就,然而其抗癌机制尚未得到系统阐明。凋亡是公认的砷剂诱导肿瘤细胞死亡的基本方式,此外自噬性细胞死亡(autophagy)、程序性坏死(necrosis)以及永久性衰老(permanent aging)等刚被人们认识的非凋亡性死亡最近也被报道在砷剂杀灭肿瘤细胞的作用中扮演重要角色。多种细胞死亡模式的发现对砷剂抗癌机制的深入研究和临床应用具有极其重要的意义。本文结合最新研究成果,对As2O3诱导肿瘤细胞多种死亡模式(凋亡、自噬性死亡、程序性坏死及永久性衰老)的分子机制进行了综述,并分析了在砷剂治癌过程中如何利用不同死亡模式的协同作用最大程度地提高其临床应用价值,以期为未来As2O3抗癌和增敏机制的深入研究提出新的研究方向。
Arsenic trioxide (As2O3) has achieved some success in the treatment of hematological tumors and various solid tumors. However, its anticancer mechanism has not been elucidated systematically. Apoptosis is a well-established basic way of arsenic-induced tumor cell death. In addition, the newly recognized non-apoptotic death such as autophagy, necrosis and permanent aging It has also recently been reported that arsenic plays an important role in the killing of tumor cells. The discovery of a variety of cell death patterns is of great importance for further research and clinical application of arsenic anticancer mechanisms. In this review, we summarize the molecular mechanisms of As2O3-induced multiple death patterns of tumor cells (apoptosis, autophagic death, programmed necrosis and permanent aging) and analyze how arsenic is administered Using the synergistic effect of different death patterns to maximize its clinical value, with a view to a new research direction for the future in-depth study of As2O3 anti-cancer and sensitization mechanisms.