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Conventional protein kinase C isoforms are not essential for cellular proliferation of a T cell lymphoma line
Author(s) -
Long Aideen,
Kelleher Dermot
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)80662-e
Subject(s) - protein kinase c , pkc alpha , staurosporine , gene isoform , cell culture , cell growth , microbiology and biotechnology , biology , kinase , chemistry , biochemistry , gene , genetics
The role of conventional protein kinase C (PKC) isoforms in the proliferation of a T cell lymphoma line was investigated. PKC isozyme‐deficient cell lines were generated from HuT 78 which expresses PKC isoforms α, β, ϵ and ζ. The first of these, K‐4, expresses PKC α, ϵ and ζ but not β. L‐2, a mutant of K‐4, expresses PKC α and ζ, but expresses neither PKC α, β, γ, ϵ nor ζ when cultured continuously in PMA (L‐2/PMA). All four cell lines continued to proliferate although at reduced rates in the presence of the PKC inhibitors staurosporine and H‐7. K‐4 and HuT 78 undergo growth arrest when activated with PMA (rate of proliferation decreases by 76 and 95%, respectively). While PMA‐induced growth arrest occurs in L‐2 cells which possess PKC α and ζ, PMA‐induced growth arrest does not occur in L‐2/PMA which is deficient in these isoforms. As these cell lines continue to proliferate in the presence of PKC inhibitors and since proliferation occurs in the absence of PKC isoforms (L‐2/PMA), the results suggest that neither conventional PKC nor the ϵ and ζ isoforms are essential for proliferation of these cells. These data further suggest that PKC α and/or ζ may be involved in PMA‐induced growth arrest.