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Carcinogenesis Advance Access published online on October 24, 2003
Carcinogenesis, doi:10.1093/carcin/bgh003
© 2003 by Oxford University Press
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© 2003 Oxford University Press

CANCER BIOLOGY

RING protein Trim32 associated with skin carcinogenesis has anti-apoptotic and E3-ubiquitin ligase properties

Elizabeth J. Horn 1, Amador Albor 2, Yuangang Liu 2, Sally El-Hizawi 2, Gretchen E. Vanderbeek 2, Melissa Babcock 2, G. Tim Bowden 3, Henry Hennings 4, Guillermina Lozano 5, Wendy C. Weinberg 6, and Molly Kulesz-Martin 7*

1 Department of Dermatology, Oregon Health & Science University, Portland, Oregon, OR 97239, USA; Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, State University of New York at Buffalo, Buffalo, New York, NY 14263
2 Department of Dermatology, Oregon Health & Science University, Portland, Oregon, OR 97239, USA
3 Department of Radiation Oncology, University of Arizona, Tucson, Arizona, AZ 85724, USA
4 Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute/National Institutes of Health, Bethesda, Maryland, MD 20892, USA
5 Department of Molecular Genetics, The University of Texas M.D. Anderson Cancer Center Houston, TX 77030, USA
6 Laboratory of Immunobiology, U.S. Food and Drug Administration, Rockville MD 20857, USA
7 Department of Dermatology and Cell & Developmental Biology, Oregon Health & Science University, Portland, Oregon, OR 97239, USA; Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, State University of New York at Buffalo, Buffalo, New York, NY 14263, USA

* Corresponding author. E-mail: kuleszma{at}ohsu.edu.

Received 29 May 2003 ; revised 29 September 2003 ; accepted 14 October 2003

Abstract

Tripartite motif protein 32, Trim32, mRNA and protein expression was elevated in independently transformed and tumorigenic keratinocytes of a mouse epidermal carcinogenesis model, in UVB-induced squamous cell carcinomas, and in approximately 20-25% of chemically induced mouse papillomas and human head and neck squamous cell carcinomas. This suggests that elevated Trim32 expression occurs frequently in experimental epidermal carcinogenesis and is relevant to human cancer. Transduced Trim32 increased colony number in an epidermal in vitro transformation assay and epidermal thickening in vivo when skin-grafted to athymic nu/nu mice. These effects were not associated with proliferation and were not sufficient for tumorigenesis, even with TPA treatment or defects in the tumor suppressor p53. However, transduced Trim32 inhibited the synergistic effect of TNF{alpha} on UVB-induced apoptosis of keratinocytes in vitro and the apoptotic response of keratinocyte grafts exposed to UVB-light in vivo. Consistent with its RING domain, Trim32 exhibited characteristics of E3-ubiquitin ligases, including being ubiquitylated itself and interacting with ubiquitylated proteins, with increases in these properties following treatment of cultured keratinocytes with TNF{alpha}/UVB. Interestingly, missense point mutation of human TRIM32 has been reported in Limb-Girdle Muscular Dystrophy Type 2H, an autosomal recessive disease. We propose a model in which Trim32 activities as an E3-ubiquitin ligase favor initiated cell survival in carcinogenesis by blocking UVB-induced TNF{alpha} apoptotic signaling.

keratinocyte carcinogenesis, TNF{alpha}, UVB, apoptosis, E3-ligase
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