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E1a is an exogenous in vivo tumour suppressor

AuthorsCimas, Francisco J.; Callejas-Valera, Juan L.; García-Olmo, Dolores C.; Hernández-Losa, Javier; Melgar-Rojas, Pedro; Ruiz-Hidalgo, María J.; Pascual-Serra, Raquel; Ortega-Muelas, Marta; Roche, Olga; Marcos, Pilar; Garcia-Gil, Elena; Fernández-Aroca, Diego M.; Ramón y Cajal, Santiago; Gutkind, J. Silvio; Sánchez-Prieto, Ricardo
Tumour suppressor
Transgenic mouse
Skin carcinogenesis
Gene therapy
Issue Date28-Jul-2017
CitationCancer Letters 399: 74-81 (2017)
AbstractThe E1a gene from adenovirus has become a major tool in cancer research. Since the discovery of E1a, it has been proposed to be an oncogene, becoming a key element in the model of cooperation between oncogenes. However, E1a's in vivo behaviour is consistent with a tumour suppressor gene, due to the block/delay observed in different xenograft models. To clarify this interesting controversy, we have evaluated the effect of the E1a 13s isoform from adenovirus 5 in vivo. Initially, a conventional xenograft approach was performed using previously unreported HCT116 and B16-F10 cells, showing a clear anti-tumour effect regardless of the mouse's immunological background (immunosuppressed/immunocompetent). Next, we engineered a transgenic mouse model in which inducible E1a 13s expression was under the control of cytokeratin 5 to avoid side effects during embryonic development. Our results show that E1a is able to block chemical skin carcinogenesis, showing an anti-tumour effect. The present report demonstrates the in vivo anti-tumour effect of E1a, showing that the in vitro oncogenic role of E1a cannot be extrapolated in vivo, supporting its future use in gene therapy approaches.
Publisher version (URL)https://doi.org/10.1016/j.canlet.2017.04.010
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