Abstract
Arsenite is the most likely carcinogenic form of arsenic in the environment. Previously, expression cloning for cDNAs whose overexpression confers arsenite-resistance in Chinese hamster V79 cells identified two genes: fau and a novel gene, asr2. The fau gene encodes a ubiquitin-like protein (here called FUBI) fused to the ribosomal S30 protein. Since the expression of the fox sequence (antisense to fau) increased the tumorigenicity of a mouse sarcoma virus, it was proposed that fau might be a tumor suppressor gene. We intended to test its ability to block arsenite-induced transformation of human osteogenic sarcoma (HOS) cells to anchorage-independence. Instead, we found that overexpressing fau itself was able to transform HOS cells. When the two domains were expressed separately, only FUBI was transforming and only the S30 domain conferred arsenite resistance. An incidental finding was the transforming activity of the selectable marker, hyg. FUBI belongs to the ubiquitin-like protein group that is capable of forming conjugates to other proteins, although none have so far been identified. Alternatively, FUBI may act as a substitute or inhibitor of ubiquitin, to which it is most closely related, or to close ubiquitin-like relatives UCRP, FAT10, and/or Nedd8.
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Acknowledgements
We thank Eleanor Cordisco for her expert help in document preparation. This work was supported by United States Public Health Service Grants R01 ES09252 and P42 ES10344, and is part of NYU's Nelson Institute of Environmental Medicine Center programs supported by Grants ES00260 from NIEHS and CA16087 from NCI.
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Rossman, T., Visalli, M. & Komissarova, E. fau and its ubiquitin-like domain (FUBI) transforms human osteogenic sarcoma (HOS) cells to anchorage-independence. Oncogene 22, 1817–1821 (2003). https://doi.org/10.1038/sj.onc.1206283
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DOI: https://doi.org/10.1038/sj.onc.1206283
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