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: Nitric oxide ( NO ) shows tumoricidal activity . We had previously reported that NO downregulates the phosphatidylinositol-3-kinase/Akt pathway , but upregulates the MEK/ERK pathway downstream of growth factor signaling . We hypothesized that NO donor and MEK inhibitor in combination synergistically inhibit the viability of cancer cells compared to either NO donor or MEK inhibitor alone . We determined the effects of S-nitrosoglutathione ( GSNO , NO-donor ) and U0126 ( MEK inhibitor ) on insulin-like growth factor-I ( IGF-I ) and epidermal growth factor ( EGF ) signaling , proliferation and invasion in cancer cell lines . GSNO inhibits phosphorylation of IGF-I receptor ( IGF-IR ) , EGF receptor ( EGFR ) and Akt , but upregulates ERK1/2 phosphorylation in MIAPaCa-2 and HCT-116 cells after stimulation by IGF-I and EGF . On the other hand , U0126 inhibits phosphorylation of ERK1/2 , but upregulates phosphorylation of IGF-IR and EGFR in MIAPaCa-2 and HCT-116 cells . The combination of GSNO and U0126 downregulates phosphorylation of IGF-IR , EGFR , Akt and ERK1/2 after stimulation by IGF-I and EGF . GSNO as well as U0126 , inhibits the proliferation of MIAPaCa-2 , HCT-116 , Panc-1 , MCF-7 , HT-29 and AGS cells in a dose-dependent manner . GSNO and U0126 in combination synergistically inhibit proliferation and invasion of cancer cells . These results indicate that the combined treatment of NO donor and MEK inhibitor may be promising in cancer therapy .
    OUTPUT:

agent
sustaining proliferative signaling;activating invasion and metastasis
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: Nitric oxide ( NO ) shows tumoricidal activity . We had previously reported that NO downregulates the phosphatidylinositol-3-kinase/Akt pathway , but upregulates the MEK/ERK pathway downstream of growth factor signaling . We hypothesized that NO donor and MEK inhibitor in combination synergistically inhibit the viability of cancer cells compared to either NO donor or MEK inhibitor alone . We determined the effects of S-nitrosoglutathione ( GSNO , NO-donor ) and U0126 ( MEK inhibitor ) on insulin-like growth factor-I ( IGF-I ) and epidermal growth factor ( EGF ) signaling , proliferation and invasion in cancer cell lines . GSNO inhibits phosphorylation of IGF-I receptor ( IGF-IR ) , EGF receptor ( EGFR ) and Akt , but upregulates ERK1/2 phosphorylation in MIAPaCa-2 and HCT-116 cells after stimulation by IGF-I and EGF . On the other hand , U0126 inhibits phosphorylation of ERK1/2 , but upregulates phosphorylation of IGF-IR and EGFR in MIAPaCa-2 and HCT-116 cells . The combination of GSNO and U0126 downregulates phosphorylation of IGF-IR , EGFR , Akt and ERK1/2 after stimulation by IGF-I and EGF . GSNO as well as U0126 , inhibits the proliferation of MIAPaCa-2 , HCT-116 , Panc-1 , MCF-7 , HT-29 and AGS cells in a dose-dependent manner . GSNO and U0126 in combination synergistically inhibit proliferation and invasion of cancer cells . These results indicate that the combined treatment of NO donor and MEK inhibitor may be promising in cancer therapy .
    OUTPUT:
