human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: Ruthenium(II) methylimidazole complexes , with the general formula [ Ru(MeIm)(4)(Nâ¢N)](2+) ( Nâ¢N=tip ( RMC1 ) , iip ( RMC2 ) , dppz ( RMC3 ) , dpq ( RMC4 ) ; MeIm=1-methylimidazole , tip=2-(thiophene-2-yl)-1H-imidazo [ 4,5-f ] [ 1,10]phenanthroline , iip=2-(1H-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 .
    OUTPUT:

agent
resisting cell death
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: Ruthenium(II) methylimidazole complexes , with the general formula [ Ru(MeIm)(4)(Nâ¢N)](2+) ( Nâ¢N=tip ( RMC1 ) , iip ( RMC2 ) , dppz ( RMC3 ) , dpq ( RMC4 ) ; MeIm=1-methylimidazole , tip=2-(thiophene-2-yl)-1H-imidazo [ 4,5-f ] [ 1,10]phenanthroline , iip=2-(1H-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 .
    OUTPUT:
