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Carcinogenesis Advance Access originally published online on October 24, 2003
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Carcinogenesis, Vol. 25, No. 2, 157-167, February 2004
© Oxford University Press; all rights reserved

CANCER BIOLOGY

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

Elizabeth J. Horn1,2, Amador Albor1, Yuangang Liu1, Sally El-Hizawi1, Gretchen E. Vanderbeek1, Melissa Babcock1, G. Tim Bowden3, Henry Hennings4, Guillermina Lozano5, Wendy C. Weinberg6 and Molly Kulesz-Martin1,2,7

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

Tripartite motif protein 32, Trim32, mRNA and protein expression was elevated in independently transformed and tumorigenic keratinocytes of a mouse epidermal carcinogenesis model, in ultraviolet B (UVB)-induced squamous cell carcinomas (SCC), and in ~20–25% of chemically induced mouse papillomas and human head and neck SCCs. 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 12-O-tetradecanoylphorbol-13-acetate treatment or defects in the tumor suppressor p53. However, transduced Trim32 inhibited the synergistic effect of tumor necrosis factor {alpha} (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.


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