(-)-表没食子酸儿茶素（EGCG）的抗癌特性通过诱导凋亡、抑制细胞增殖和组蛋白去乙酰化酶来介导。稳定的细胞FLICE抑制蛋白（c-FLIP）/Ku70复合物在细胞质中的积累通过中断外源性凋亡通路抑制凋亡。在本研究中，我们通过解离c-FLIP/Ku70复合物来评估EGCG在胃癌（GC）细胞中的抗癌作用。用EGCG或其拮抗剂MG149处理MKN-45细胞24小时后，通过流式细胞术和定量反转录聚合酶链反应评估凋亡。用西方博莱特和免疫荧光法分析c-FLIP和Ku70的蛋白表达。通过亚细胞分离和共免疫沉淀研究c-FLIP/Ku70复合物的解离以及Ku70的转位。EGCG诱导MKN-45细胞凋亡，上调P53和P21的表达，下调c-Myc和Cyclin D1的表达，同时在S和G2/M检查点引起细胞周期停滞。此外，EGCG处理抑制c-FLIP和Ku70的表达，降低它们的相互作用，同时增加Ku70在细胞核中的含量。通过解离c-FLIP/Ku70复合物，EGCG可以作为传统HDAC抑制剂的替代组分，用于诱导GC细胞凋亡。因此，将EGCG与其他癌症治疗方案结合可能会获得更好的治疗效果。© 2023 The Authors. 由细胞与分子医学基金会和约翰威利和儿Sons有限公司出版的《细胞与分子医学杂志》发表。

Anti-cancer properties of (-)-epigallocatechin-3-gallate (EGCG) are mediated via apoptosis induction, as well as inhibition of cell proliferation and histone deacetylase. Accumulation of stabilized cellular FLICE-inhibitory protein (c-FLIP)/Ku70 complex in the cytoplasm inhibits apoptosis through interruption of extrinsic apoptosis pathway. In this study, we evaluated the anti-cancer role of EGCG in gastric cancer (GC) cells through dissociation of c-FLIP/Ku70 complex. MKN-45 cells were treated with EGCG or its antagonist MG149 for 24 h. Apoptosis was evaluated by flow cytometry and quantitative RT-PCR. Protein expression of c-FLIP and Ku70 was analysed using western blot and immunofluorescence. Dissociation of c-FLIP/Ku70 complex as well as Ku70 translocation were studied by sub-cellular fractionation and co-immunoprecipitation. EGCG induced apoptosis in MKN-45 cells with substantial up-regulation of P53 and P21, down-regulation of c-Myc and Cyclin D1 as well as cell cycle arrest in S and G2/M check points. Moreover, EGCG treatment suppressed the expression of c-FLIP and Ku70, decreased their interaction while increasing the Ku70 nuclear content. By dissociating the c-FLIP/Ku70 complex, EGCG could be an alternative component to the conventional HDAC inhibitors in order to induce apoptosis in GC cells. Thus, its combination with other cancer therapy protocols could result in a better therapeutic outcome.© 2023 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.