抗癌活性已被广泛研究。在本文中，三个配体 2-(6-溴苯并[d][1,3]二氧杂环己烷-5-基)-1H-咪唑并[4,5-f][1,10]菲咯啉 (BDIP)、2-( 7-甲氧基苯并[d][1,3]二氧杂环戊烯-5-基)-1H-咪唑并[4,5-f][1,10]菲咯啉 (MDIP), 2-(6-硝基苯并[d][1, 3]间二氧杂环戊醇-5-基)-1H-咪唑并[4,5-f][1,10]菲咯啉 (NDIP) 及其铱(III)络合物: [Ir(ppy)2(BDIP)](PF6) (合成了 ppy = 去质子化 2-苯基吡啶，3a)、[Ir(ppy)2(MDIP)](PF6) (3b) 和 [Ir(ppy)2(NDIP)](PF6) (3c)。使用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物测试 3a、3b、3c 对 Huh7、A549、BEL-7402、HepG2、HeLa 和非癌症 NIH3T3 的细胞毒性（MTT）法。 MTT测试结果清楚地表明，这些复合物对Huh7、BEL-7402、HepG2和HeLa（A549细胞除外）表现出中等或非细胞毒性。为了提高抗癌功效，我们用白光照射细胞和复合物的混合物30分钟，复合物的抗癌活性大大增强。特别是，3a和3b表现出增强的抑制A549细胞增殖的能力，IC50（半数最大抑制浓度）值分别为0.7±0.3μM和1.8±0.1μM。细胞摄取表明3a和3b可以在细胞质中积累。伤口愈合和集落形成表明3a和3b显着阻碍S期细胞迁移和生长。该复合物打开线粒体通透性转换孔(MPTP)通道，引起膜电位降低、细胞色素C释放、caspase 3激活，最终导致细胞凋亡。此外，3a和3b会引起自噬，增加脂质过氧化并导致铁死亡。此外，3a 和 3b 还会增加钙网蛋白 (CRT)、高迁移率族蛋白 1 (HMGB1)、热休克蛋白 70 (HSP70) 的表达，从而诱导免疫原性细胞死亡。版权所有 © 2024 Elsevier Inc. 保留所有权利。

Anticancer activity has been extensively studies. In this article, three ligands 2-(6-bromobenzo[d][1,3]dioxol-5-yl)-1H-imidazo[4,5-f][1,10]phenanthroline (BDIP), 2-(7-methoxybenzo[d][1,3]dioxol-5-yl)-1H-imidazo[4,5-f][1,10]phenanthroline (MDIP), 2-(6-nitrobenzo[d][1,3]dioxol-5-yl)-1H-imidazo[4,5-f][1,10]phenanthroline (NDIP) and their iridium(III) complexes: [Ir(ppy)2(BDIP)](PF6) (ppy = deprotonated 2-phenylpyridine, 3a), [Ir(ppy)2(MDIP)](PF6) (3b) and [Ir(ppy)2(NDIP)](PF6) (3c) were synthesized. The cytotoxicity of 3a, 3b, 3c against Huh7, A549, BEL-7402, HepG2, HeLa, and non-cancer NIH3T3 was tested using 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) method. The results obtained from the MTT test stated clearly that these complexes demonstrated moderate or non-cytotoxicity toward Huh7, BEL-7402, HepG2 and HeLa except A549 cells. To improve the anticancer efficacy, we used white light to irradiate the mixture of cells and complexes for 30 min, the anticancer activity of the complexes was greatly enhanced. Particularly, 3a and 3b exhibited heightened capability to inhibit A549 cells proliferation with IC50 (half maximal inhibitory concentration) values of 0.7 ± 0.3 μM and 1.8 ± 0.1 μM, respectively. Cellular uptake has shown that 3a and 3b can be accumulated in the cytoplasm. Wound healing and colony forming showed that 3a and 3b significantly hinder the cell migration and growth in the S phase. The complexes open mitochondrial permeability transition pore (MPTP) channel and cause the decrease of membrane potential, release of cytochrome C, activation of caspase 3, and finally lead to apoptosis. In addition, 3a and 3b cause autophagy, increase the lipid peroxidation and lead to ferroptosis. Also, 3a and 3b increase the expression of calreticulin (CRT), high mobility group box 1 (HMGB1), heat shock protein 70 (HSP70), thereby inducing immunogenic cell death.Copyright © 2024 Elsevier Inc. All rights reserved.