PHORBOL DIESTER AND EPIDERMAL GROWTH-FACTOR RECEPTORS IN 12-O-TETRADECANOYLPHORBOL-13-ACETATE-RESISTANT AND 12-O-TETRADECANOYLPHORBOL-13-ACETATE-SENSITIVE MOUSE EPIDERMAL-CELLS

  • 1 January 1982
    • journal article
    • research article
    • Vol. 42  (8) , 3093-3097
Abstract
Several cell variants were isolated from promotable mouse JB6 epidermal cells which are resistant either to mitogenic stimulation at quiescence or to promotion of anchorage independence by 12-O-tetradecanoylphorbol-13 acetate (TPA). Such resistant variants would be expected to lack 1 or more steps in the TPA response pathway leading to mitogenesis or promotion of tumor cell phenotype. This report is concerned with determining whether resistance is attributable to lack of receptors for phorbol diesters or epidermal growth factor (EGF, a potential mediator) or to absence of receptor down modulation following ligand binding. Neither lack of phorbol diester receptors nor absence of down modulation can be demonstrated in the TPA-resistant variants. The phorbol ester binding affinity is also not altered in the resistant variant. The presence of EGF receptors cannot be an absolute requirement for TPA promotion sensitivity since 3 of the TPA-promotable cell lines lack available EGF receptors. Lack of EGF receptors may account for TPA mitogen resistance in at least 3 of 4 resistant variants. The TPA-induced EGF binding decrease occurs in both sensitive and resistant variants. Thus, phorbol diester binding and receptor down modulation remain as possible required events in mitogenic and promotion responses to TPA. EGF receptors are clearly not necessary for TPA promotion of anchorage independence in JB6 cells, but may mediate mitogenic stimulation of these cells by TPA.

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