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Volumn 10, Issue 1, 2000, Pages 81-93

Tumor suppressor genes

Author keywords

[No Author keywords available]

Indexed keywords

CASPASE; CYCLIN D1; PROTEIN P53; RETINOBLASTOMA PROTEIN; SMAD PROTEIN;

EID: 0034002662     PISSN: 0959437X     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0959-437X(99)00041-6     Document Type: Review
Times cited : (145)

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    • Fan, S.1    Wang, J.2    Yuan, R.3    Ma, Y.4    Meng, Q.5    Erdos, M.R.6    Pestell, R.G.7    Yuan, F.8    Auborn, K.J.9    Goldberg, I.D.10    Rosen, E.M.11
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    • 0033615352 scopus 로고    scopus 로고
    • PPARδ is an APC-regulated target of non-steroidal anti-inflammatory drugs
    • The authors identified PPARδ as an APC-regulated gene by SAGE methodology and were able to confirm that induction of APC in colorectal cell lines repressed expression of PPARδ but not other members of the PPAR family. The inhibition of PPARδ by APC was mediated by β-catenin/Tcf-4 binding sites in the promoter of PPARδ. NSAIDS also inhibited PPARδ by interfering with the DNA-binding activity of PPARδ/RXRα dimers and over-expression of PPARδ could partially repress programmed cell death induced by NSAIDS. A role for PPAR receptors in regulating the growth of colonic epithelium has already been proposed [29] and the data presented here further support a key role for these transcriptional regulators in colorectal tumorigenesis. The critical targets of the PPARs in growth control remain to be identified but as factors regulated by the APC tumor suppressor gene, NSAIDS and dietary lipids, the function of PPARs requires great attention.
    • He T-C., Chan T.A., Vogelstein B., Kinzler K.W. PPARδ is an APC-regulated target of non-steroidal anti-inflammatory drugs. Cell. 99:1999;335-345. The authors identified PPARδ as an APC-regulated gene by SAGE methodology and were able to confirm that induction of APC in colorectal cell lines repressed expression of PPARδ but not other members of the PPAR family. The inhibition of PPARδ by APC was mediated by β-catenin/Tcf-4 binding sites in the promoter of PPARδ. NSAIDS also inhibited PPARδ by interfering with the DNA-binding activity of PPARδ/RXRα dimers and over-expression of PPARδ could partially repress programmed cell death induced by NSAIDS. A role for PPAR receptors in regulating the growth of colonic epithelium has already been proposed [29] and the data presented here further support a key role for these transcriptional regulators in colorectal tumorigenesis. The critical targets of the PPARs in growth control remain to be identified but as factors regulated by the APC tumor suppressor gene, NSAIDS and dietary lipids, the function of PPARs requires great attention.
    • (1999) Cell , vol.99 , pp. 335-345
    • He, T.-C.1    Chan, T.A.2    Vogelstein, B.3    Kinzler, K.W.4


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.