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mDia1 targets v-Src to the cell periphery and facilitates cell transformation, tumorigenesis, and invasion

Masahiro Tanji1, Toshimasa Ishizaki, Saman Ebrahimi

  • 1Department of Pharmacology, Kyoto University Faculty of Medicine, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan.

Molecular and Cellular Biology
|August 4, 2010
PubMed

Insights

The Rho-mDia1 pathway is crucial for cancer development. Its absence suppresses Src-induced cell transformation, tumorigenesis, and invasion by regulating actin cytoskeleton and Src localization.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Biochemistry

Background:

  • The small GTPase Rho regulates cell morphogenesis via actin cytoskeleton remodeling.
  • Rho is overexpressed in many cancers, but its role in oncogenesis is unclear.
  • mDia1, a Rho effector, produces straight actin filaments.

Purpose of the Study:

  • To investigate the involvement and mechanism of the Rho-mDia1 pathway in Src-induced oncogenesis.
  • To determine how mDia1 deficiency affects cell transformation and tumor progression.

Main Methods:

  • Transduction of mDia1-deficient mouse embryonic fibroblasts with temperature-sensitive v-Src.
  • Analysis of actin filament formation, v-Src localization, and tyrosine phosphorylation.
  • In vitro transformation assays (focus and soft agar colony formation).
  • In vivo tumorigenesis and invasion assays in nude mice.

Main Results:

  • mDia1 deficiency suppressed actin filament formation and v-Src translocation to focal adhesions.
  • Morphological transformation, podosome formation, and tyrosine phosphorylation were impaired in mDia1-deficient cells.
  • mDia1-deficient cells exhibited reduced in vitro transformation and suppressed in vivo tumorigenesis and invasion.

Conclusions:

  • The Rho-mDia1 pathway facilitates malignant transformation and invasion.
  • mDia1 is essential for regulating the actin cytoskeleton and Src localization at the cell periphery.
  • Targeting the Rho-mDia1 pathway could offer therapeutic strategies for cancers with c-Src overexpression.

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