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: Past studies have shown that amplified insulin-like growth factor 1 ( IGF1)/IGF1 receptor ( IGF1-R ) signalling has an important role in colorectal cancer ( CRC ) development , progression and resistance to treatment . In this report , we demonstrate that downregulation of microRNA-497 ( miR-497 ) as a result of DNA copy number reduction is involved in upregulation of IGF1-R in CRC cells . MiR-497 and miR-195 of the miR-15/16/195/424/497 family that share the same 3 ' untranslated region ( 3'UTR ) binding seed sequence and are predicted to target IGF1-R were concurrently downregulated in the majority of CRC tissues relative to paired adjacent normal mucosa . However , only overexpression of miR-497 led to suppression of the IGF1-R 3'UTR activity and downregulation of the endogenous IGF1-R protein in CRC cells . This was associated with inhibition of cell survival , proliferation and invasion , and increased sensitivity to apoptosis induced by various stimuli including the chemotherapeutic drugs cisplatin and 5-fluorouracil , and the death ligand tumour necrosis factor-related apoptosis-inducing ligand . The biological effect of miR-497 on CRC cells was largely mediated by inhibition of phosphatidylinositol 3-kinase/Akt signalling , as overexpression of an active form of Akt reversed its impact on cell survival and proliferation , recapitulating the effect of overexpression of IGF1-R . Downregulation of miR-497 and miR-195 appeared to associate with copy number loss of a segment of chromosome 17p13.1 , where these miRs are located at proximity . Similarly to miR-195 , the members of the same miR family , miR-424 that was upregulated , and miR-15a , miR-15b and miR-16 that were unaltered in expression in CRC tissues compared with paired adjacent normal mucosa , did not appear to have a role in regulating the expression of IGF1-R . Taken together , these results identify downregulation of miR-497 as an important mechanism of upregulation of IGF1-R in CRC cells that contributes to malignancy of CRC.Oncogene advance online publication , 18 June 2012 ; doi:10.1038/onc.2012.214 .
    OUTPUT:

agent
sustaining proliferative signaling;activating invasion and metastasis;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: Past studies have shown that amplified insulin-like growth factor 1 ( IGF1)/IGF1 receptor ( IGF1-R ) signalling has an important role in colorectal cancer ( CRC ) development , progression and resistance to treatment . In this report , we demonstrate that downregulation of microRNA-497 ( miR-497 ) as a result of DNA copy number reduction is involved in upregulation of IGF1-R in CRC cells . MiR-497 and miR-195 of the miR-15/16/195/424/497 family that share the same 3 ' untranslated region ( 3'UTR ) binding seed sequence and are predicted to target IGF1-R were concurrently downregulated in the majority of CRC tissues relative to paired adjacent normal mucosa . However , only overexpression of miR-497 led to suppression of the IGF1-R 3'UTR activity and downregulation of the endogenous IGF1-R protein in CRC cells . This was associated with inhibition of cell survival , proliferation and invasion , and increased sensitivity to apoptosis induced by various stimuli including the chemotherapeutic drugs cisplatin and 5-fluorouracil , and the death ligand tumour necrosis factor-related apoptosis-inducing ligand . The biological effect of miR-497 on CRC cells was largely mediated by inhibition of phosphatidylinositol 3-kinase/Akt signalling , as overexpression of an active form of Akt reversed its impact on cell survival and proliferation , recapitulating the effect of overexpression of IGF1-R . Downregulation of miR-497 and miR-195 appeared to associate with copy number loss of a segment of chromosome 17p13.1 , where these miRs are located at proximity . Similarly to miR-195 , the members of the same miR family , miR-424 that was upregulated , and miR-15a , miR-15b and miR-16 that were unaltered in expression in CRC tissues compared with paired adjacent normal mucosa , did not appear to have a role in regulating the expression of IGF1-R . Taken together , these results identify downregulation of miR-497 as an important mechanism of upregulation of IGF1-R in CRC cells that contributes to malignancy of CRC.Oncogene advance online publication , 18 June 2012 ; doi:10.1038/onc.2012.214 .
    OUTPUT:
