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: 1-(3-C-ethynyl-beta-d-ribo-pentofuranosyl)cytosine ( ECyd ) is a ribose-modified nucleoside analog of cytidine with potent anticancer activity in several cancers . The main antitumor mechanism of this promising RNA-directed nucleoside anti-metabolite is efficient blockade of RNA synthesis in cancer cells . Here , we examined the therapeutic potential of this RNA-directed anti-metabolite in in vitro models of nasopharyngeal cancer ( NPC ) . In a panel of 6 NPC cell lines , ECyd effectively inhibited cellular proliferation at nM concentrations ( IC(50) : approximately 13-44nM ) . Moreover , cisplatin-resistant NPC cells were highly sensitive to ECyd ( at nM concentration ) . The ECyd-mediated growth inhibition was associated with G(2)/M cell cycle arrest , PARP cleavage ( a hallmark of apoptosis ) and Bcl-2 downregulation , indicating induction of apoptosis by ECyd in NPC cells . Unexpectedly , ECyd-induced significant downregulation of TIGAR , a newly described dual regulator of apoptosis and glycolysis . More importantly , this novel action of ECyd on TIGAR was accompanied by marked depletion of NADPH , the major reducing power critically required for cell proliferation and survival . We hypothesized that ECyd-induced TIGAR downregulation was crucially involved in the antitumor activity of ECyd . Indeed , overexpression of TIGAR was able to rescue NPC cells from ECyd-induced growth inhibition , demonstrating a novel mechanistic action of ECyd on TIGAR . We demonstrated for the first time that an RNA-directed nucleoside analog , ECyd , exerts its antitumor activity via downregulation of a novel regulator of apoptosis , TIGAR . Moreover , ECyd may represent a novel therapy for NPC .
    OUTPUT:

agent
resisting cell death;cellular energetics
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.
    ###
    INPUT: 1-(3-C-ethynyl-beta-d-ribo-pentofuranosyl)cytosine ( ECyd ) is a ribose-modified nucleoside analog of cytidine with potent anticancer activity in several cancers . The main antitumor mechanism of this promising RNA-directed nucleoside anti-metabolite is efficient blockade of RNA synthesis in cancer cells . Here , we examined the therapeutic potential of this RNA-directed anti-metabolite in in vitro models of nasopharyngeal cancer ( NPC ) . In a panel of 6 NPC cell lines , ECyd effectively inhibited cellular proliferation at nM concentrations ( IC(50) : approximately 13-44nM ) . Moreover , cisplatin-resistant NPC cells were highly sensitive to ECyd ( at nM concentration ) . The ECyd-mediated growth inhibition was associated with G(2)/M cell cycle arrest , PARP cleavage ( a hallmark of apoptosis ) and Bcl-2 downregulation , indicating induction of apoptosis by ECyd in NPC cells . Unexpectedly , ECyd-induced significant downregulation of TIGAR , a newly described dual regulator of apoptosis and glycolysis . More importantly , this novel action of ECyd on TIGAR was accompanied by marked depletion of NADPH , the major reducing power critically required for cell proliferation and survival . We hypothesized that ECyd-induced TIGAR downregulation was crucially involved in the antitumor activity of ECyd . Indeed , overexpression of TIGAR was able to rescue NPC cells from ECyd-induced growth inhibition , demonstrating a novel mechanistic action of ECyd on TIGAR . We demonstrated for the first time that an RNA-directed nucleoside analog , ECyd , exerts its antitumor activity via downregulation of a novel regulator of apoptosis , TIGAR . Moreover , ECyd may represent a novel therapy for NPC .
    OUTPUT:
