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Abrogation of IL-3 dependent growth requires a functional v-src gene product: evidence for an autocrine growth cycle

S M Anderson1, P M Carroll, F D Lee

  • 1Department of Pathology, SUNY, Stony Brook 11794.

Oncogene
|March 1, 1990
PubMed

Insights

The v-src oncogene enables myeloid progenitor cells to grow without growth factors. Infected cells release an unidentified growth factor, suggesting a novel autocrine mechanism in cancer.

Area of Science:

  • Oncogene research
  • Cellular signaling
  • Hematopoiesis

Background:

  • Interleukin-3 (IL-3) is crucial for myeloid progenitor cell growth.
  • The v-src oncogene is known to disrupt normal cellular regulation.
  • Understanding oncogene-induced transformation is key to cancer research.

Purpose of the Study:

  • To investigate if the v-src oncogene can override IL-3 dependent growth in 32D c13 cells.
  • To identify the mechanism by which v-src confers growth factor independence.
  • To characterize any secreted growth factors from v-src transformed cells.

Main Methods:

  • Infection of 32D c13 cells with murine retroviruses encoding v-src.
  • Isolation and characterization of growth factor-independent clones.
  • Use of temperature-sensitive v-src mutants to confirm direct responsibility.
  • Analysis of secreted factors and mRNA from infected cells.

Main Results:

  • v-src oncogene confers growth factor independence on 32D c13 cells.
  • Temperature-sensitive mutants confirm v-src directly causes this independence.
  • v-src infected cells secrete a factor that stimulates normal cell proliferation.
  • The secreted factor is not a currently identified hematopoietic growth factor.

Conclusions:

  • The v-src oncogene directly abrogates the need for IL-3 in myeloid progenitor cells.
  • v-src transformation leads to autocrine production of an unknown growth-promoting factor.
  • This finding suggests a novel pathway for oncogene-induced cell proliferation.

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