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.
    ###
    INPUT: We previously demonstrated that downregulation of protein kinase CKII induces cellular senescence in human colon cancer HCT116 cells . To investigate the role of microRNAs ( miRNAs ) in CKII downregulation during senescence , we employed computational algorithms . Four miRNAs ( miR-186 , miR-216b , miR-337-3p , and miR-760 ) were predicted to be miRNAs against CKIIÎ± mRNA . Mimics of all four miRNAs jointly downregulated CKIIÎ± expression in HCT116 cells . Reporter analysis and RT-PCR have suggested that these four miRNAs may stimulate degradation of CKIIÎ± mRNA by targeting its 3 ' untranslated regions ( UTRs ) . The four miRNA mimics increased senescent-associated Î²-galactosidase ( SA-Î²-gal ) staining , p53 and p21(Cip1/WAF1) expression , and reactive oxygen species ( ROS ) production . In contrast , concomitant knockdown of the four miRNAs by antisense inhibitors increased the CKIIÎ± protein level and suppressed CKII inhibition-mediated senescence . Finally , CKIIÎ± overexpression antagonized senescence induced by the four miRNA mimics . Therefore , the present results show that miR-186 , miR-216b , miR-337-3p , and miR-760 cooperatively promote cellular senescence through the p53-p21(Cip1/WAF1) pathway by CKII downregulation-mediated ROS production in HCT116 cells .
    OUTPUT:

agent
enabling replicative immortality;tumor promoting inflammation
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: We previously demonstrated that downregulation of protein kinase CKII induces cellular senescence in human colon cancer HCT116 cells . To investigate the role of microRNAs ( miRNAs ) in CKII downregulation during senescence , we employed computational algorithms . Four miRNAs ( miR-186 , miR-216b , miR-337-3p , and miR-760 ) were predicted to be miRNAs against CKIIÎ± mRNA . Mimics of all four miRNAs jointly downregulated CKIIÎ± expression in HCT116 cells . Reporter analysis and RT-PCR have suggested that these four miRNAs may stimulate degradation of CKIIÎ± mRNA by targeting its 3 ' untranslated regions ( UTRs ) . The four miRNA mimics increased senescent-associated Î²-galactosidase ( SA-Î²-gal ) staining , p53 and p21(Cip1/WAF1) expression , and reactive oxygen species ( ROS ) production . In contrast , concomitant knockdown of the four miRNAs by antisense inhibitors increased the CKIIÎ± protein level and suppressed CKII inhibition-mediated senescence . Finally , CKIIÎ± overexpression antagonized senescence induced by the four miRNA mimics . Therefore , the present results show that miR-186 , miR-216b , miR-337-3p , and miR-760 cooperatively promote cellular senescence through the p53-p21(Cip1/WAF1) pathway by CKII downregulation-mediated ROS production in HCT116 cells .
    OUTPUT:
