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Putrescine and spermidine uptake is regulated by proliferation and dexamethasone treatment in AR4‐2J cells
Author(s) -
Nicolet Thierry,
Scemama JeanLuc,
Pradayrol Lucien,
Berthélémy Philippe,
Seva Catherine,
Vaysse Nicole
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910490418
Subject(s) - spermidine , putrescine , polyamine , spermine , intracellular , biology , cell growth , cell , microbiology and biotechnology , biochemistry , enzyme
Polyamines are essential for cell growth and differentiation. Their specific uptake contributes to the regulation of intracellular polyamine levels. In this study, we describe the modulation of this transport mechanism in a rat tumoral pancreatic acinar cell line (AR4‐2J) and analyze the transport system characteristics of the normal rat pancreatic acini. Normal acini had a common carrier for spermidine and spermine, like AR4‐2J cells, but not a specific putrescine carrier. Intracellular polyamine deprivation enhanced putrescine and spermidine uptake of AR4‐2J cells with no modification of polyamine carrier affinity. Uptake was modulated during growth and decreased for both polyamines at confluence. AR4‐2J cell differentiation with dexamethasone prevented cell proliferation and diminished uptake of both putrescine and spermidine without affecting their respective carrier affinities. Our data show, first, that the polyamine transport system could be modulated by polyamine metabolism with no change in its affinity characteristics. Second, in rat pancreatic acinar cells, neoplastic transformation was partly characterized by induction of a high‐affinity putrescine carrier. This phenotype was not reversed by dexamethasone‐induced cell differentiation.