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: Epigenetic deregulation of gene expression has a role in the initiation and progression of prostate cancer ( PCa ) . The histone methyltransferase MMSET/WHSC1 ( Multiple Myeloma SET domain ) is overexpressed in a number of metastatic tumors , but its mechanism of action has not been defined . In this work , we found that PCa cell lines expressed significantly higher levels of MMSET compared with immortalized , non-transformed prostate cells . Knockdown experiments showed that , in metastatic PCa cell lines , dimethylation of lysine 36 and trimethylation of lysine 27 on histone H3 ( H3K36me2 and H3K27me3 , respectively ) depended on MMSET expression , whereas depletion of MMSET in benign prostatic cells did not affect chromatin modifications . Knockdown of MMSET in DU145 and PC-3 tumor cells decreased cell proliferation , colony formation in soft agar and strikingly diminished cell migration and invasion . Conversely , overexpression of MMSET in immortalized , non-transformed RWPE-1 cells promoted cell migration and invasion , accompanied by an epithelial-mesenchymal transition ( EMT ) . Among a panel of EMT-promoting genes analyzed , TWIST1 expression was strongly activated in response to MMSET . Chromatin immunoprecipitation analysis demonstrated that MMSET binds to the TWIST1 locus and leads to an increase in H3K36me2 , suggesting a direct role of MMSET in the regulation of this gene . Depletion of TWIST1 in MMSET-overexpressing RWPE-1 cells blocked cell invasion and EMT , indicating that TWIST1 was a critical target of MMSET , responsible for the acquisition of an invasive phenotype . Collectively , these data suggest that MMSET has a role in PCa pathogenesis and progression through epigenetic regulation of metastasis-related genes .
    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: Epigenetic deregulation of gene expression has a role in the initiation and progression of prostate cancer ( PCa ) . The histone methyltransferase MMSET/WHSC1 ( Multiple Myeloma SET domain ) is overexpressed in a number of metastatic tumors , but its mechanism of action has not been defined . In this work , we found that PCa cell lines expressed significantly higher levels of MMSET compared with immortalized , non-transformed prostate cells . Knockdown experiments showed that , in metastatic PCa cell lines , dimethylation of lysine 36 and trimethylation of lysine 27 on histone H3 ( H3K36me2 and H3K27me3 , respectively ) depended on MMSET expression , whereas depletion of MMSET in benign prostatic cells did not affect chromatin modifications . Knockdown of MMSET in DU145 and PC-3 tumor cells decreased cell proliferation , colony formation in soft agar and strikingly diminished cell migration and invasion . Conversely , overexpression of MMSET in immortalized , non-transformed RWPE-1 cells promoted cell migration and invasion , accompanied by an epithelial-mesenchymal transition ( EMT ) . Among a panel of EMT-promoting genes analyzed , TWIST1 expression was strongly activated in response to MMSET . Chromatin immunoprecipitation analysis demonstrated that MMSET binds to the TWIST1 locus and leads to an increase in H3K36me2 , suggesting a direct role of MMSET in the regulation of this gene . Depletion of TWIST1 in MMSET-overexpressing RWPE-1 cells blocked cell invasion and EMT , indicating that TWIST1 was a critical target of MMSET , responsible for the acquisition of an invasive phenotype . Collectively , these data suggest that MMSET has a role in PCa pathogenesis and progression through epigenetic regulation of metastasis-related genes .
    OUTPUT:
