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: Peroxisome proliferator activated receptor Î³ ( PPARÎ³ ) , a subgroup of ligand-activated nuclear receptors , plays critical roles in cell cycle regulation , differentiation , apoptosis and invasion . PPARÎ³ is involved in tumorigenesis and is a potent target for cancer therapy . PPARÎ³ transactivation of KLF4 has been demonstrated in various studies ; however , how PPARÎ³ regulates KLF4 expression is not clear . In this study , we revealed that PPARÎ³ regulates the expression of KLF4 by binding directly to the PPAR response element ( PPRE ) within the KLF4 promoter . The PPRE resided at -1657bp to -1669bp upstream of the KLF4 ATG codon , which is essential for the transactivation of TGZ-induced KLF4 expression . Furthermore , we found that stable silencing of KLF4 obviously suppressed the G1/S arrest and anti-proliferation effects induced by PPARÎ³ ligands . Taken together , our data indicated that upregulating KLF4 upon PPARÎ³ activation is mediated through PPRE in KLF4 promoter , thus providing further insights into PPARÎ³ signal transduction pathway as well as a novel cancer therapeutic strategy .
    OUTPUT:

agent
evading growth suppressors;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: Peroxisome proliferator activated receptor Î³ ( PPARÎ³ ) , a subgroup of ligand-activated nuclear receptors , plays critical roles in cell cycle regulation , differentiation , apoptosis and invasion . PPARÎ³ is involved in tumorigenesis and is a potent target for cancer therapy . PPARÎ³ transactivation of KLF4 has been demonstrated in various studies ; however , how PPARÎ³ regulates KLF4 expression is not clear . In this study , we revealed that PPARÎ³ regulates the expression of KLF4 by binding directly to the PPAR response element ( PPRE ) within the KLF4 promoter . The PPRE resided at -1657bp to -1669bp upstream of the KLF4 ATG codon , which is essential for the transactivation of TGZ-induced KLF4 expression . Furthermore , we found that stable silencing of KLF4 obviously suppressed the G1/S arrest and anti-proliferation effects induced by PPARÎ³ ligands . Taken together , our data indicated that upregulating KLF4 upon PPARÎ³ activation is mediated through PPRE in KLF4 promoter , thus providing further insights into PPARÎ³ signal transduction pathway as well as a novel cancer therapeutic strategy .
    OUTPUT:
