Antitumor activity studies of iridium (III) polypyridine complexes-loaded liposomes against gastric tumor cell in vitro
| Autor: | Zhi-Tong Huang, Fu-Li Xie, Si-Hong Liu, Jian-Wei Zhu, Hui-Hua Xu, Qi-Feng Guo, Lan Bai, Yong Wu, Qing-Qin Long |
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| Rok vydání: | 2021 |
| Předmět: |
Pyridines
Cell Antineoplastic Agents Apoptosis Iridium Biochemistry Inorganic Chemistry HeLa Mice Cell Movement Coordination Complexes Stomach Neoplasms Cell Line Tumor medicine Autophagy Animals Humans Cytotoxicity Protein kinase B Cell Proliferation Membrane Potential Mitochondrial Liposome Drug Carriers biology Cell growth Chemistry biology.organism_classification Molecular biology G1 Phase Cell Cycle Checkpoints Mitochondria medicine.anatomical_structure Cancer cell Liposomes NIH 3T3 Cells Reactive Oxygen Species |
| Zdroj: | Journal of inorganic biochemistry. 225 |
| ISSN: | 1873-3344 |
| Popis: | Two iridium (III) polypyridine complexes [Ir(ppy)2(BIP)]PF6 (ppy = 2-phenylpyridine, BIP = 2-biphenyl-1H-imidazo[4,5-f][1,10]phenanthroline, Ir1), [Ir(piq)2(BIP)]PF6 (piq = 1-phenylisoquinoline, Ir2) and their liposomes Ir1lipo and Ir2lipo were synthesized and characterized. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to evaluate cytotoxic activity against several cancer cells (A549, HepG2, SGC-7901, Bel-7402, HeLa) and non-cancer cell (mouse embryonic fibroblast, NIH3T3). The results showed that Ir1lipo displays the high cytotoxicity toward SGC-7901 with IC50 value of 5.8 ± 0.2 μM, while the complexes have no cytotoxicity toward A549, HepG2, Bel-7402 and HeLa cells. The cell colony demonstrated that the iridium (III) complexes-loaded liposomes can inhibit cell proliferation, induce cell cycle arrest at G0/G1 phase. Moreover, they also cause autophagy, induce a decrease of mitochondrial membrane potential and increase intracellular reactive oxygen species (ROS) content. These results suggest that the complexes encapsulated liposomes Ir1lipo and Ir2lipo inhibit the growth of SGC-7901 cells through a ROS-mediated mitochondrial dysfunction and activating the PI3K (phosphoinositide-3 kinase)/ AKT (protein kinase B) signaling pathways. |
| Databáze: | OpenAIRE |
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