Marine Bioprocess Research Center, Department of Chemistry, Pukyong National University, Busan 608-737, Korea.
Int J Mol Sci. 2013 Jan 24;14(2):2334-54. doi: 10.3390/ijms14022334.
Inhibition of apoptosis leads to activation of cell survival factors (e.g., AKT) causes continuous cell proliferation in cancer. Apoptosis, the major form of cellular suicide, is central to various physiological processes and the maintenance of homeostasis in multicellular organisms. A number of discoveries have clarified the molecular mechanism of apoptosis, thus clarifying the link between apoptosis and cell survival factors, which has a therapeutic outcome. Induction of apoptosis and inhibition of cell survival by anticancer agents has been shown to correlate with tumor response. Cellular damage induces growth arrest and tumor suppression by inducing apoptosis, necrosis and senescence; the mechanism of cell death depends on the magnitude of DNA damage following exposure to various anticancer agents. Apoptosis is mainly regulated by cell survival and proliferating signaling molecules. As a new therapeutic strategy, alternative types of cell death might be exploited to control and eradicate cancer cells. This review discusses the signaling of apoptosis and cell survival, as well as the potential contribution of marine bioactive compounds, suggesting that new therapeutic strategies might follow.
凋亡抑制导致细胞存活因子(如 AKT)的激活会导致癌症中细胞的持续增殖。凋亡是细胞自杀的主要形式,是多细胞生物中各种生理过程和维持内稳态的核心。许多发现阐明了细胞凋亡的分子机制,从而阐明了凋亡与细胞存活因子之间的联系,这具有治疗效果。抗癌药物诱导凋亡和抑制细胞存活与肿瘤反应相关。细胞损伤通过诱导凋亡、坏死和衰老来抑制生长和肿瘤抑制;细胞死亡的机制取决于暴露于各种抗癌药物后 DNA 损伤的程度。凋亡主要受细胞存活和增殖信号分子的调节。作为一种新的治疗策略,可能会利用其他类型的细胞死亡来控制和消灭癌细胞。本文综述了细胞凋亡和细胞存活的信号转导,以及海洋生物活性化合物的潜在贡献,表明可能会出现新的治疗策略。