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Deficiency of caveolin-1 in Apc(min/+) mice promotes colorectal tumorigenesis

Teresa Friedrich1, Birgit Richter, Timo Gaiser

  • 1Department of Internal Medicine II, Universitätsmedizin Mannheim, Medical Faculty Mannheim, Heidelberg University, D-68167 Mannheim, Germany.

Carcinogenesis
|May 4, 2013
PubMed

Insights

Loss of Caveolin-1 (Cav1) accelerates colorectal cancer (CRC) development in mice. Activating PPARg may offer new CRC treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Caveolin-1 (Cav1) is a protein involved in cell signaling pathways.
  • Cav1's role in colorectal cancer (CRC) tumorigenesis in vivo was previously unknown.

Purpose of the Study:

  • To investigate the in vivo role of Cav1 in colorectal cancer (CRC).
  • To determine if Cav1 deficiency accelerates CRC development.

Main Methods:

  • Generated a novel mouse model by crossing Apc(min/+) mice with Cav1 knockout (Cav1-/-) mice.
  • Analyzed tumor incidence and characteristics in Apc(min/+) Cav1-/- mice compared to controls.
  • Examined gene expression and protein localization related to Ras, wingless, and PPARg signaling.

Main Results:

  • Apc(min/+) Cav1-/- mice exhibited a higher incidence of large, invasive adenocarcinomas in the distal colon and rectum.
  • Intratumoral Ras and wingless signaling were elevated, while PPARg activity was reduced.
  • The PPARg-agonist rosiglitazone inhibited tumor formation regardless of Cav1 status and increased expression of docking protein-1.

Conclusions:

  • Co-deficiency of Cav1 and adenomatous polyposis coli facilitates CRC formation.
  • PPARg activation presents a potential therapeutic strategy for colorectal cancer treatment.

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