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Analysis of transcriptional activation of a cyclic AMP response element by 2,6,10,14‐tetramethylpentadecane (pristane) in JB6 mouse epidermal cells
Author(s) -
Banbura Marcin,
AcklandBerglund Cathleen,
Lee SoongHo,
Hamernik Deborah,
Jones Clinton
Publication year - 1994
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.2940110406
Subject(s) - pristane , biology , microbiology and biotechnology , biochemistry , chemistry , hydrocarbon , organic chemistry
Abstract Pristane is a naturally occurring isoprenoid that is believed to be derived from the phytyl moity of chlorophyll. Thus, it is not surprising that pristane is present in many common fruits and vegetables. Furthermore, pristane can be detected in the tissues of fish and mammals. In animal models using rodents, pristane canfunction as a potent tumour promoter. At the molecular level, pristane can induce changes in the plasma membrane, alter the conformation of chromatin, and selectively activate gene expression. Addition of pristane to a mouse epidermal cell line (JB6 P+) allows these cells to grow in an anchorage‐independent manner. In contrast, JB6 P‐cells are not transformed by pristane. Our study was undertaken to correlate transformation of P+ cells with changes induced by pristane. Transcriptional activation of a cyclic AMP response element (CRE) was in duced by pristane in P+ and P‐cells. Point mutations in the CRE abolished activation by pristane, thus indicating that an intact CRE was necessary for pristane activation. In P+ cells, pristane repressed phosphodiesterase activity. However, protein kinase A was activated by pristance in P+ and P‐cells. Taken together, these results indicated pristane induced novel changes in P+cells that in turn may facilitate neoplastic transformation.©1994 Wiley‐Liss, Inc.