Abstract：
Mitosis of somatic cells produces a daughter cell. Apoptosis, a naturally programmed cellular death mechanism, kills abnormal cells produced by mitosis. Cancer can develop when this equilibrium is disrupted, either by an upsurge in cell propagation or a reduction in tissue demise. Cancer therapy aims to cause cancer cells to die while inflicting little harm to healthy cells. This review of apoptotic mechanism processes improves our understanding of how certain malignancies begin and develop. The current cancer treatments can operate either by inducing apoptosis or causing direct cell damage. An insight into the resistance to apoptosis may explicate why malignancy treatments fail in some situations. New therapies grounded on our understanding of apoptotic processes are being developed to induce apoptosis of cancer cells while limiting the simultaneous death of normal cells. Various biological activities require redox equilibrium to function properly. Antineoplastic medications that cause oxidative stress by raising ROS and blocking antioxidant mechanisms have recently attracted much interest. The rapid accumulation of ROS impairs redox balance and damages cancer cells severely. Here, we discuss ROS-instigating malignancy therapy and the antineoplastic mechanism used by prooxidative drugs.
摘要：
体细胞的有丝分裂产生子细胞。细胞凋亡,一种自然编程的细胞死亡机制，杀死有丝分裂产生的异常细胞。当这种平衡被破坏时，癌症就会发展，要么是细胞增殖的激增，要么是组织死亡的减少。癌症治疗旨在导致癌细胞死亡，同时对健康细胞造成很小的伤害。对凋亡机制过程的回顾提高了我们对某些恶性肿瘤如何开始和发展的理解。目前的癌症治疗可以通过诱导细胞凋亡或引起直接的细胞损伤来操作。对细胞凋亡抗性的洞察可以解释为什么恶性肿瘤治疗在某些情况下失败。基于我们对凋亡过程的理解的新疗法正在开发中，以诱导癌细胞凋亡，同时限制正常细胞的同时死亡。各种生物活性需要氧化还原平衡才能正常发挥作用。通过提高ROS和阻断抗氧化机制引起氧化应激的抗肿瘤药物最近引起了很多兴趣。ROS的快速积累损害氧化还原平衡并严重损害癌细胞。这里,我们讨论了刺激ROS的恶性肿瘤治疗和促氧化药物使用的抗肿瘤机制。
