Literature DB >> 2541502

AP1/jun function is differentially induced in promotion-sensitive and resistant JB6 cells.

L R Bernstein1, N H Colburn.   

Abstract

Tumor promoters may bring about events that lead to neoplastic transformation by inducing specific promotion-relevant effector genes. Functional activation of the transacting transcription factor AP-1 by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) may play an essential role in this process. Clonal genetic variants of mouse epidermal JB6 cells that are genetically susceptible (P+) or resistant (P-) to promotion of transformation by TPA were transfected with 3XTRE-CAT, a construct that has AP-1 cis-enhancer sequences attached to a reporter gene encoding chloramphenicol acetyltransferase (CAT). Transfected JB6 P+, but not P- variants, showed TPA-inducible CAT synthesis. Epidermal growth factor, another transformation promoter in JB6 cells, also caused P+ specific induction of CAT gene expression. These results demonstrate an association between induced AP-1 function and sensitivity to promotion of neoplastic transformation.

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Year:  1989        PMID: 2541502     DOI: 10.1126/science.2541502

Source DB:  PubMed          Journal:  Science        ISSN: 0036-8075            Impact factor:   47.728


  56 in total

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5.  The transactivating domain of the c-Jun proto-oncoprotein is required for cotransformation of rat embryo cells.

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Review 8.  The role of AP-1, NF-kappaB and ROS/NOS in skin carcinogenesis: the JB6 model is predictive.

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9.  Blocking of tumor promoter-induced AP-1 activity inhibits induced transformation in JB6 mouse epidermal cells.

Authors:  Z Dong; M J Birrer; R G Watts; L M Matrisian; N H Colburn
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10.  The role of the c-Jun N-terminal Kinase signaling pathway in skin cancer.

Authors:  Jennifer Y Zhang; Maria Angelica Selim
Journal:  Am J Cancer Res       Date:  2012-11-20       Impact factor: 6.166

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