首页|Ruthenium methylimidazole complexes induced apoptosis in lung cancer A549 cells through intrinsic mitochondrial pathway
Ruthenium methylimidazole complexes induced apoptosis in lung cancer A549 cells through intrinsic mitochondrial pathway
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Elsevier
Ruthenium(II) methylimidazole complexes, with the general formula [Ru(MeIm)4(N⌒N)]~(2+) (N⌒N = tip (RMC1), iip (RMC2), dppz (RMC3), dpq (RMC4); Melm = 1-methylimidazole, tip = 2-(thiophene-2-yl)-lH-imidazo [4,5-f] [1,10]phenanthroline, iip = 2-(lH-imidazol-4-yl)-1H-imidazo [4,5-f] [1,10]phenanthroline, dppz = dipyrido[3,2-a:2',3'-c]phenazine, dpq = pyrazino [2,3-f] [1,10]phenanthroline), were synthesized and characterized. As determined by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay, these complexes displayed potent anti-proliferation activity against various cancer cells. RMC1 inhibited the growth of A549 (human lung adenocarcinoma) lung cells through induction of apoptotic cell death, as evidenced by the accumulation of cell population in sub-G1 phase. RMC1 also induced the depletion of mitochondrial membrane potential in A549 cells by regulating the expression of pro-survival and pro-apoptotic Bcl-2 family members. Another experiment showed that Bid protein was also activated by RMC1, which implied that RMC1 could existed two pathways crosstalk, namely, have exogenous death receptor signaling pathway. These results demonstrated that RMC1 induced cancer cell death by acting on both mitochondrial and death receptor apoptotic pathways, suggesting that RMC1 could be a candidate for further evaluation as a chemotherapeutic agent against human cancers.
rutheniumapoptosiscaspaseBcl-2mitochondria
Xiaoxin Yang、Lanmei Chen、Yanan Liu、Yongguang Yang、Tianfeng Chen、Wenjie Zheng、Jie Liu、Qing-Yu He
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Department of Chemistry, Jinan University, Guangzhou 510632, China
School of Pharmacy, Guangdong Medical College, Zhanjiang 524023, China
Institute of Life and Health Engineering, Jinan University, Guangzhou 510632, China
NETL
NSTL
Elsevier
