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: RKIP-1 is a metastasis suppressor that is frequently downregulated in aggressive cancers . However , the consequences of RKIP loss in primary or immortalized cells have not yet been explored . Using HEK-293 RKIP depleted ( termed HEK-499 ) and Flp-In T-Rex-293 RKIP inducible cell lines combined with whole transcriptome analysis , we show that RKIP-1 silencing accelerates DNA synthesis and G1/S transition entry by inducing the expression of cdc6 , MCM 2 , 4 , 6 , 7 , cdc45L , cyclin D2 , cyclin E2 , cyclin D1 , SKP2 and the downregulation of p21(cip1) . Moreover , RKIP depletion accelerates the time from nuclear envelop breakdown ( NEB ) to anaphase markedly , while the upregulation of RKIP shortened the NEB to anaphase time . We show that RKIP depletion induces the expression of NEK6 , a molecule known to enhance G2/M transition , and down-regulates G2/M checkpoint molecules like Aurora B , cyclin G1 and sertuin that slow the G2/M transition time . These subtle changes in the kinetics of the cell cycle culminate in a higher proliferation rate of HEK-499 compared to control cells . Finally , we show that RKIP depletion enhances cellular motility by inducing the expression/stabilization of Î²-catenin , vimentin , MET and PAK1 . Overall , our data suggest that modulation of the cell cycle checkpoints and motility by RKIP may be fundamental to its metastasis suppressive function in cancer and that RKIP role in a cell is more intricate and diverse than previously thought .
    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: RKIP-1 is a metastasis suppressor that is frequently downregulated in aggressive cancers . However , the consequences of RKIP loss in primary or immortalized cells have not yet been explored . Using HEK-293 RKIP depleted ( termed HEK-499 ) and Flp-In T-Rex-293 RKIP inducible cell lines combined with whole transcriptome analysis , we show that RKIP-1 silencing accelerates DNA synthesis and G1/S transition entry by inducing the expression of cdc6 , MCM 2 , 4 , 6 , 7 , cdc45L , cyclin D2 , cyclin E2 , cyclin D1 , SKP2 and the downregulation of p21(cip1) . Moreover , RKIP depletion accelerates the time from nuclear envelop breakdown ( NEB ) to anaphase markedly , while the upregulation of RKIP shortened the NEB to anaphase time . We show that RKIP depletion induces the expression of NEK6 , a molecule known to enhance G2/M transition , and down-regulates G2/M checkpoint molecules like Aurora B , cyclin G1 and sertuin that slow the G2/M transition time . These subtle changes in the kinetics of the cell cycle culminate in a higher proliferation rate of HEK-499 compared to control cells . Finally , we show that RKIP depletion enhances cellular motility by inducing the expression/stabilization of Î²-catenin , vimentin , MET and PAK1 . Overall , our data suggest that modulation of the cell cycle checkpoints and motility by RKIP may be fundamental to its metastasis suppressive function in cancer and that RKIP role in a cell is more intricate and diverse than previously thought .
    OUTPUT:
