Hmga1 null mice are less susceptible to chemically induced skin carcinogenesis

Rosa Visone1, Rodolfo Iuliano, Dario Palmieri

  • 1Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università degli Studi di Napoli Federico II, via Pansini, 5, 80131, Naples, Italy.

European Journal of Cancer (Oxford, England : 1990)
|December 25, 2007
PubMed

Insights

Mice lacking the HMGA1 gene (Hmga1-/-) showed reduced susceptibility to chemically induced skin cancer. These findings highlight HMGA1 proteins

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • High mobility group AT-hook 1 (HMGA1) proteins are implicated in carcinogenesis and are overexpressed in many human cancers.
  • Inhibiting HMGA1 expression can prevent malignant cell transformation and induce cancer cell death.

Purpose of the Study:

  • To investigate the role of HMGA1 proteins in in vivo carcinogenesis.
  • To assess the tumor susceptibility of Hmga1 knockout mice in a chemical skin carcinogenesis model.

Main Methods:

  • A two-stage chemical skin carcinogenesis protocol was employed.
  • Tumor susceptibility was compared between wild-type and Hmga1 knockout (Hmga1-/-) mice.

Main Results:

  • Hmga1-/- mice displayed a reduced number and delayed onset of skin papillomas compared to wild-type mice.
  • The progression of skin papillomas to carcinomas was significantly lower in Hmga1-/- mice (5%) versus wild-type mice (18%).

Conclusions:

  • HMGA1 proteins are essential for in vivo skin carcinogenesis.
  • Hmga1 knockout mice exhibit decreased susceptibility to chemically induced skin tumors, suggesting HMGA1 as a potential therapeutic target.