EFFECTS OF SPECIFIC FATTY-ACIDS ON PROLACTIN-INDUCED NB2 LYMPHOMA CELL-PROLIFERATION

Citation
Pw. Sylvester et al., EFFECTS OF SPECIFIC FATTY-ACIDS ON PROLACTIN-INDUCED NB2 LYMPHOMA CELL-PROLIFERATION, Life sciences, 52(24), 1993, pp. 1977-1984
Citations number
25
Categorie Soggetti
Biology,"Medicine, Research & Experimental
Journal title
ISSN journal
00243205
Volume
52
Issue
24
Year of publication
1993
Pages
1977 - 1984
Database
ISI
SICI code
0024-3205(1993)52:24<1977:EOSFOP>2.0.ZU;2-S
Abstract
Nb2 rat lymphoma cells are dependent on prolactin (PRL) for growth. Me mbrane lipid composition of Nb2 cells undergoes rapid modification whe n these cells are grown in culture media supplemented with specific fa tty acids. Since the actions of PRL are mediated through specific memb rane receptors, the following studies were conducted to characterize t he lipid-dependent events involved in fatty acid modulation of PRL-ind uced cell proliferation. Nb2 cells were grown in suspension cultures i n control or fatty acid-supplemented media, in the presence of various doses of PRL. PRL-induced cell growth was significantly enhanced by a rachidonate, but significantly attenuated by stearate supplementation of the culture media. A direct relationship was observed between the c oncentration of specific fatty acid added to the culture media and the magnitude with which this fatty acid was incorporated into Nb2 cell m embranes, as determined by gas chromatography. Acute treatment with ph orbol ester enhanced Nb2 cell growth in control media and reversed the attenuating effects of membrane stearic acid enrichment. However, PRL -induced Nb2 cell growth was similar with or without the presence of p horbol ester, when cells were grown in media supplemented with arachid onate. Addition of protein kinase C (PKC) inhibitors to control and fa tty acid-supplemented media resulted in a dose-dependent inhibition of PRL-indUced Nb2 cell proliferation. These results suggest that lipid modulation of Nb2 mitogenic-responsiveness to PRL is mediated through alterations in PKC activation.