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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
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Mechanism of induction of transforming growth factor-beta type II receptor gene expression by v-Src in murine myeloid

S H Park1, M C Birchenall-Roberts, Y Yi

  • 1Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892-5055, USA.

Cell Growth & Differentiation : the Molecular Biology Journal of the American Association for Cancer Research
|February 24, 2001
PubMed

Insights

v-Src transformation increases sensitivity to transforming growth factor (TGF)-beta1 by upregulating the TGF-beta type II receptor (TGF-beta RII) gene. This involves v-Src activating specific promoter elements, enhancing TGF-beta RII expression in myeloid cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Hematopoiesis

Background:

  • Transforming growth factor (TGF)-beta1 is crucial for hematopoiesis.
  • v-Src-transformed myeloid cells exhibit heightened sensitivity to TGF-beta1 inhibition compared to wild-type cells.

Purpose of the Study:

  • To investigate the molecular mechanisms behind the increased TGF-beta1 sensitivity in v-Src-transformed myeloid cells.
  • To examine the role of the TGF-beta type II receptor (TGF-beta RII) gene expression.

Main Methods:

  • Northern blot analysis to assess TGF-beta RII transcript levels.
  • Reporter gene assays to measure TGF-beta RII promoter activity.
  • DNA transfection and electrophoretic mobility shift assays to identify transcription factor binding sites.

Main Results:

  • v-Src significantly increased TGF-beta RII transcript expression (8- and 6-kb species) in myeloid cell lines.
  • v-Src induced TGF-beta RII promoter activity by 23-fold.
  • v-Src activates the TGF-beta RII promoter via AP1/ATF2-like, ETS, and inverted CCAAT elements, increasing specific DNA-protein complex formation.

Conclusions:

  • v-Src oncogene upregulates TGF-beta RII gene expression.
  • v-Src enhances TGF-beta RII promoter activity through multiple regulatory elements.
  • These findings elucidate a mechanism for increased TGF-beta sensitivity in v-Src-transformed cells.

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