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MRTF-A/B suppress the oncogenic properties of v-ras- and v-src-mediated transformants

Toshiyuki Yoshio1, Tsuyoshi Morita, Masahiko Tsujii

  • 1Department of Neuroscience, Osaka University Graduate School of Medicine, Yamadaoka 2-2, Suita, Osaka 565-0871, Japan.

Carcinogenesis
|March 27, 2010
PubMed

Insights

Myocardin-related transcription factors (MRTF)-A/B regulate actin cytoskeleton proteins. Restoring MRTF-A/B function in cancer cells suppressed tumor growth, invasion, and metastasis, suggesting therapeutic potential.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Myocardin-related transcription factor (MRTF)-A and MRTF-B are co-activators of serum response factor (SRF).
  • MRTF-A/B regulate actin cytoskeletal and focal adhesion genes, influencing cell structure and function.
  • Actin cytoskeleton organization is frequently disrupted in cancer cells.

Purpose of the Study:

  • To investigate the role of MRTF-A/B in cancer progression using rat intestinal epithelial (RIE) cell lines transformed with oncogenic ras or src.
  • To determine if restoring MRTF-A/B activity can reverse cancer-associated phenotypes and inhibit tumor growth and metastasis.

Main Methods:

  • Compared actin cytoskeletal protein levels (caldesmon, tropomyosin) and MRTF-A/B nuclear translocation in normal RIE cells versus RIE-ras and RIE-src cells.
  • Utilized transient and stable expression of constitutively active (CA) MRTF-A in transformed RIE cells.
  • Assessed morphological changes, actin cytoskeleton organization, in vitro invasiveness, anchorage-independent growth, and in vivo tumor formation and metastasis.

Main Results:

  • Transformed RIE-ras and RIE-src cells showed reduced caldesmon and tropomyosin levels and suppressed MRTF-A/B nuclear translocation, with disorganized actin cytoskeletons.
  • Transient or stable expression of CA-MRTF-A restored caldesmon and tropomyosin levels, normalized cell morphology, and improved actin cytoskeleton organization.
  • CA-MRTF-A expression significantly reduced in vitro invasiveness and anchorage-independent growth of transformed cells.
  • In vivo, CA-MRTF-A expression suppressed tumor formation and reduced liver metastases.

Conclusions:

  • MRTF-A/B play a crucial role in maintaining normal cell structure and function by regulating actin cytoskeleton dynamics.
  • Loss or suppression of MRTF-A/B activity contributes to cancer progression, including increased invasiveness and metastasis.
  • MRTF-A/B are potent repressors of cancer progression and metastasis, representing promising therapeutic targets for cancer treatment.

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