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Cold shock domain protein A represses angiogenesis and lymphangiogenesis via inhibition of serum response element

Y Saito1, H Nakagami, M Kurooka

  • 1Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, Osaka, Japan.

Oncogene
|October 16, 2007
PubMed

Insights

Mouse cold shock domain protein A (mCSDA) inhibits both blood vessel and lymphatic vessel growth. This dual-targeted therapy approach shows promise for treating cancers by repressing tumor angiogenesis and lymphangiogenesis.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Dual-targeted therapy inhibiting angiogenesis and lymphangiogenesis is a promising strategy for cancer treatment.
  • Identifying genes that inhibit both processes is crucial for developing novel anti-cancer therapies.

Purpose of the Study:

  • To identify genes encoding inhibitors of both angiogenesis and lymphangiogenesis.
  • To investigate the role of mouse cold shock domain protein A (mCSDA) in regulating endothelial cell proliferation and tumor growth.

Main Methods:

  • Utilized a cDNA library from Lewis lung carcinoma (LL/2) to identify candidate genes.
  • Evaluated growth inhibition in aortic and lymphatic endothelial cells (ECs) upon mCSDA overexpression.
  • Assessed tumor growth and EC marker expression in an LL/2 mouse model following mCSDA injection.

Main Results:

  • mCSDA overexpression significantly repressed proliferation and c-fos promoter activity in various ECs.
  • CSDA directly binds to the hypoxia response element (HRE) and serum response element (SRE), inhibiting their activity.
  • mCSDA injection significantly repressed tumor growth and decreased blood and lymphatic EC markers in vivo.

Conclusions:

  • CSDA acts as a dual inhibitor of angiogenesis and lymphangiogenesis.
  • mCSDA demonstrates potential as a therapeutic agent for repressing tumor growth by targeting both blood and lymphatic vessel formation.

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