Enforced expression of the M(r) 33,000 Pim-1 kinase enhances factor- independent survival and inhibits apoptosis in murine myeloid cells

Michael Lilly, Andrew Kraft

Research output: Contribution to journalArticle

86 Scopus citations

Abstract

Expression of the M(r) 33,000 human Pim-1 protein is induced in hematopoietic cells by a variety of growth factors and cytokines. We have introduced the human pim-1 cDNA via retroviral transduction into interleukin (IL)-3-dependent FDC-P1 cells and examined the resulting phenotype. Compared with cells infected with a neo-encoding retrovirus (FD/neo), cells infected with a pim-1-transducing virus (FD/hpim) showed longer survival or autonomous growth in suspension culture in the absence of IL-3, as well as IL-3- independent clonogenic growth in semisolid medium. The unique murine M(r) 44,000 Pim-1 protein, as well as human proteins with short C- or N-terminal truncations, also was biologically active. This effect of pim-1 expression was associated with a decrease in apoptotic cells and an increase in G0/G1- phase cells, and the increase in G0/G1-phase cells caused by enforced expression of Pim-1 was due to a decrease in apoptosis rather than to a decrease in transit of the G1-S-phase checkpoint. The Pim-1 kinase appears to function primarily as a survival factor in factor-dependent FDCP-1 cells subjected to either cytokine withdrawal or exposure to cytotoxic agents.

Original languageEnglish (US)
Pages (from-to)5348-5355
Number of pages8
JournalCancer Research
Volume57
Issue number23
StatePublished - Dec 1 1997
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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