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: MicroRNAs ( miRNAs ) are considered to be regulators of various biological processes in cancers , including the epithelial to mesenchymal transition ( EMT ) , which is a key factor in cancer metastasis . In this study , we aimed to clarify the potential roles of miR-490-3p in hepatocellular carcinoma ( HCC ) cells . Using real-time quantitative RT-PCR , we discovered that miR-490-3p was up-regulated in HCC tissues and cells compared with the adjacent non-tumor tissues and normal cells . We also found that overexpression of miR-490-3p led to an increase in cell proliferation , migration , and invasion abilities and that it contributed to EMT . The inhibition of miR-490-3p had the opposite effect on the cells . We identified ERGIC3 ( endoplasmic reticulum-Golgi intermediate compartment protein 3 ) as a direct target gene for miR-490-3p . Unlike most miRNA-mRNA interactions , miR-490-3p increased ERGIC3 mRNA and protein levels as well as the intensity of expression of the EGFP reporter gene controlled by the 3'-UTR of ERGIC3 mRNA . The up-regulation by miR-490-3p also required the participation of Ago2 . The inhibition of miR-490-3p reduced the expression of ERGIC3 . Overexpression of ERGIC3 led to the same effect on HCC cells as miR-490-3p overexpression , including EMT . Importantly , silencing ERGIC3 reversed the cellular responses mediated by miR-490-3p overexpression . In conclusion , our study indicated for the first time that miR-490-3p functioned like an oncogenic miRNA in HCC cells and that the inhibition of miR-490-3p might provide an potential treatment approach for HCC patients .
    OUTPUT:

agent
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: MicroRNAs ( miRNAs ) are considered to be regulators of various biological processes in cancers , including the epithelial to mesenchymal transition ( EMT ) , which is a key factor in cancer metastasis . In this study , we aimed to clarify the potential roles of miR-490-3p in hepatocellular carcinoma ( HCC ) cells . Using real-time quantitative RT-PCR , we discovered that miR-490-3p was up-regulated in HCC tissues and cells compared with the adjacent non-tumor tissues and normal cells . We also found that overexpression of miR-490-3p led to an increase in cell proliferation , migration , and invasion abilities and that it contributed to EMT . The inhibition of miR-490-3p had the opposite effect on the cells . We identified ERGIC3 ( endoplasmic reticulum-Golgi intermediate compartment protein 3 ) as a direct target gene for miR-490-3p . Unlike most miRNA-mRNA interactions , miR-490-3p increased ERGIC3 mRNA and protein levels as well as the intensity of expression of the EGFP reporter gene controlled by the 3'-UTR of ERGIC3 mRNA . The up-regulation by miR-490-3p also required the participation of Ago2 . The inhibition of miR-490-3p reduced the expression of ERGIC3 . Overexpression of ERGIC3 led to the same effect on HCC cells as miR-490-3p overexpression , including EMT . Importantly , silencing ERGIC3 reversed the cellular responses mediated by miR-490-3p overexpression . In conclusion , our study indicated for the first time that miR-490-3p functioned like an oncogenic miRNA in HCC cells and that the inhibition of miR-490-3p might provide an potential treatment approach for HCC patients .
    OUTPUT:
