Adenovirus E1A requires c-Ras for full neoplastic transformation or suppression of differentiation of murine preadipocytes

Anagnostopoulou, A., J. Cao, R. Arulanandam, A. Vultur and L. Raptis 2007. Adenovirus E1A requires c-Ras for full neoplastic transformation or suppression of differentiation of murine preadipocytes. Molecular Carcinogenesis. 46 (4), pp. 284-302. https://doi.org/10.1002/mc.20278

TitleAdenovirus E1A requires c-Ras for full neoplastic transformation or suppression of differentiation of murine preadipocytes
TypeJournal article
AuthorsAnagnostopoulou, A., J. Cao, R. Arulanandam, A. Vultur and L. Raptis
Abstract

We recently demonstrated that the Adenovirus-5 E1A gene products (E1A), known E2F activators, can block the differentiation of murine preadipocytes and that differentiation suppression occurs at lower levels than required for full neoplastic transformation. Progressively higher levels were accompanied by apoptosis induction. To examine the role of the cellular Ras protooncogene product (Ras) in E1A function, E1A was expressed in C3H10T½ (10T½)-derived preadipocytes rendered deficient in Ras activity by transfection with inducible or constitutive antisense ras gene constructs (Ras-knockdowns). The results showed that, although even low amounts of E1A could block the differentiation of 10T½ preadipocytes with normal Ras levels, even the highest E1A levels were unable to block the differentiation or induce transformation of Ras-knockdown preadipocytes. Ras downregulation did not affect E2F activation by E1A. Interestingly, our results further demonstrated a dramatic reduction in the levels of the E1A protein itself as differentiation progressed, with a concomitant reduction in E1A's ability to induce apoptosis as a result. These findings suggest for the first time that Ras, although cytoplasmic, is an integral component of the pathway whereby E1A, an oncoprotein believed to have primarily nuclear targets, suppresses differentiation or induces neoplastic conversion of murine preadipocytes.

JournalMolecular Carcinogenesis
Journal citation46 (4), pp. 284-302
ISSN0899-1987
1098-2744
Year2007
PublisherWiley
Digital Object Identifier (DOI)https://doi.org/10.1002/mc.20278
Web address (URL)http://dx.doi.org/10.1002/mc.20278
Publication dates
PublishedApr 2007

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