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: BACKGROUND Ginkgolic acids ( GAs ) , extracted from the seed coat of Ginkgo biloba L. Our previous study has shown that GA monomer could inhibit the growth of Hep-2 significantly and induce the fragmentation of the chromosomal DNA . To further assess the antitumor potential and turn it into a candidate new antitumor drug , the antitumor mechanism of GA was investigated . METHOD The cytotoxicity and antitumor effect of GA monomer were assayed by MTT colorimetric assay with nontumorogenic MC-3T3-E1 as well as tumorogenic Hep-2 and Tac8113 cell lines . The effect of GA monomer on the proliferation of tumor cell lines was analyzed with MTT colorimetric and CFSE labeled assay . Cell cycle distribution and measurement of the percentage of apoptotic cells were performed by flow cytometry following stained with propidium iodide , annexin V-FITC . The expression of apoptotic proteins Bcl-2 , Bax and caspase-3 was analyzed with Western blot . RESULT GA only inhibited the growth of tumorogenic cell lines in a both dose- and time-dependent manner . Tumor cells were treated with GA for 72 h , 70.53 Â± 4.54% Hep-2 and 63.5 Â± 7.2% Tca8113 cells were retarded at GO/G1 phase , and the percentage of apoptosis was 40.4 Â± 1.58 and 38.4 Â± 1.7% , respectively . GA-treated activated caspase-3 downregulated the expression of anti-apoptotic Bcl-2 protein and upregulated the expression of pro-apoptotic Bax protein , eventually leading to a decrease in the Bcl-2/Bax ratio in tumor cells . CONCLUSIONS The antitumor action of GA was due to inhibiting the proliferation in a manner of inhibiting division , retarding the progress of cell cycle and inducing apoptosis , making GA a candidate as new antitumor drug .
    OUTPUT:

agent
evading growth suppressors;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: BACKGROUND Ginkgolic acids ( GAs ) , extracted from the seed coat of Ginkgo biloba L. Our previous study has shown that GA monomer could inhibit the growth of Hep-2 significantly and induce the fragmentation of the chromosomal DNA . To further assess the antitumor potential and turn it into a candidate new antitumor drug , the antitumor mechanism of GA was investigated . METHOD The cytotoxicity and antitumor effect of GA monomer were assayed by MTT colorimetric assay with nontumorogenic MC-3T3-E1 as well as tumorogenic Hep-2 and Tac8113 cell lines . The effect of GA monomer on the proliferation of tumor cell lines was analyzed with MTT colorimetric and CFSE labeled assay . Cell cycle distribution and measurement of the percentage of apoptotic cells were performed by flow cytometry following stained with propidium iodide , annexin V-FITC . The expression of apoptotic proteins Bcl-2 , Bax and caspase-3 was analyzed with Western blot . RESULT GA only inhibited the growth of tumorogenic cell lines in a both dose- and time-dependent manner . Tumor cells were treated with GA for 72 h , 70.53 Â± 4.54% Hep-2 and 63.5 Â± 7.2% Tca8113 cells were retarded at GO/G1 phase , and the percentage of apoptosis was 40.4 Â± 1.58 and 38.4 Â± 1.7% , respectively . GA-treated activated caspase-3 downregulated the expression of anti-apoptotic Bcl-2 protein and upregulated the expression of pro-apoptotic Bax protein , eventually leading to a decrease in the Bcl-2/Bax ratio in tumor cells . CONCLUSIONS The antitumor action of GA was due to inhibiting the proliferation in a manner of inhibiting division , retarding the progress of cell cycle and inducing apoptosis , making GA a candidate as new antitumor drug .
    OUTPUT:
