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Phorbol esters can persistently replace interleukin‐2 (IL‐2) for the growth of a human IL‐2‐dependent T‐cell line
Author(s) -
Takeshita Toshikazu,
Goto Yuso,
Nakamura Masataka,
Fujii Masahiro,
Iwami Masafumi,
Hinuma Yorio,
Sugamura Kazuo
Publication year - 1988
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041360215
Subject(s) - protein kinase c , autocrine signalling , cell culture , phorbol , tetradecanoylphorbol acetate , interleukin 2 , clone (java method) , cell growth , microbiology and biotechnology , growth factor , cytokine , biology , chemistry , signal transduction , biochemistry , receptor , immunology , gene , genetics
A selected clone from an IL‐2‐dependent human T‐cell line was persistently propagated in the presence of phorbol esters with the ability to activate protein kinase C (PKC), such as 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) or phorbol‐12,13‐dibutylate (PDBu). Thus, a TPA(PDBu)‐dependent T‐cell line, designated TPA‐Mat, was established from IL‐2‐dependent T cells. The TPA‐dependency of TPA‐Mat was not lost during cultivation for more than a year in the presence of TPA, and TPA‐Mat cells still showed IL‐2‐dependent growth. However, the TPA (PDBu)‐dependent growth of TPA‐Mat did not seem to be mediated by an autocrine mechanism of IL‐2 or by any other growth factor production, because these factors were not detected in TPA‐Mat cell supernatants. Therefore, the phorbol esters substituted for IL‐2 and may be directly involved in transduction of growth signals in TPA‐Mat cells. Although activity of PKC was down‐regulated, messenger ribonucleic acid (mRNA) of the PKC β‐gene was detected in TPA‐Mat cells was stimulated not only by phorbol esters but also by nonphorbol ester tumor promoters with the ability to activate PKC. These observations suggest that the sustained activation of PKC by the phorbol esters could induce continuous growth of the IL‐2‐dependent TPA‐Mat cells.