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: Heat shock protein 27 ( Hsp27 ) is emerging as a promising therapeutic target for treatment of various cancers . Although the role of Hsp27 in protection from stress-induced intrinsic cell death has been relatively well studied , its role in Fas ( death domain containing member of the tumor necrosis factor receptor superfamily)-induced apoptosis and cell proliferation remains underappreciated . Here , we show that Hsp27 silencing induces dual coordinated effects , resulting in inhibition of cell proliferation and sensitization of cells to Fas-induced apoptosis through regulation of PEA-15 ( 15-kDa phospho-enriched protein in astrocytes ) . We demonstrate that Hsp27 silencing suppresses proliferation by causing PEA-15 to bind and sequester extracellular signal-regulated kinase ( ERK ) , resulting in reduced translocation of ERK to the nucleus . Concurrently , Hsp27 silencing promotes Fas-induced apoptosis by inducing PEA-15 to release Fas-associating protein with a novel death domain ( FADD ) , thus allowing FADD to participate in death receptor signaling . Conversely , Hsp27 overexpression promotes cell proliferation and suppresses Fas-induced apoptosis . Furthermore , we show that Hsp27 regulation of PEA-15 activity occurs in an Akt-dependent manner . Significantly , Hsp27 silencing in a panel of phosphatase and tensin homolog on chromosome 10 ( PTEN ) wild-type or null cell lines , and in LNCaP cells that inducibly express PTEN , resulted in selective growth inhibition of PTEN-deficient cancer cells . These data identify a dual coordinated role of Hsp27 in cell proliferation and Fas-induced apoptosis via Akt and PEA-15 , and indicate that improved clinical responses to Hsp27-targeted therapy may be achieved by stratifying patient populations based on tumor PTEN expression .
    OUTPUT:

agent
resisting cell death;sustaining proliferative signaling
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: Heat shock protein 27 ( Hsp27 ) is emerging as a promising therapeutic target for treatment of various cancers . Although the role of Hsp27 in protection from stress-induced intrinsic cell death has been relatively well studied , its role in Fas ( death domain containing member of the tumor necrosis factor receptor superfamily)-induced apoptosis and cell proliferation remains underappreciated . Here , we show that Hsp27 silencing induces dual coordinated effects , resulting in inhibition of cell proliferation and sensitization of cells to Fas-induced apoptosis through regulation of PEA-15 ( 15-kDa phospho-enriched protein in astrocytes ) . We demonstrate that Hsp27 silencing suppresses proliferation by causing PEA-15 to bind and sequester extracellular signal-regulated kinase ( ERK ) , resulting in reduced translocation of ERK to the nucleus . Concurrently , Hsp27 silencing promotes Fas-induced apoptosis by inducing PEA-15 to release Fas-associating protein with a novel death domain ( FADD ) , thus allowing FADD to participate in death receptor signaling . Conversely , Hsp27 overexpression promotes cell proliferation and suppresses Fas-induced apoptosis . Furthermore , we show that Hsp27 regulation of PEA-15 activity occurs in an Akt-dependent manner . Significantly , Hsp27 silencing in a panel of phosphatase and tensin homolog on chromosome 10 ( PTEN ) wild-type or null cell lines , and in LNCaP cells that inducibly express PTEN , resulted in selective growth inhibition of PTEN-deficient cancer cells . These data identify a dual coordinated role of Hsp27 in cell proliferation and Fas-induced apoptosis via Akt and PEA-15 , and indicate that improved clinical responses to Hsp27-targeted therapy may be achieved by stratifying patient populations based on tumor PTEN expression .
    OUTPUT:
