Malignant transformation by cyclin E and Ha-Ras correlates with lower sensitivity towards induction of cell death but requires functional Myc ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1997-11

AUTHORS

Kirsten Haas, Christian Johannes, Christoph Geisen, Thorsten Schmidt, Holger Karsunky, Sabine Blass-Kampmann, Günter Obe, Tarik Möröy

ABSTRACT

We demonstrate in this paper that the G1 phase specific cell cycle regulator cyclin E is able to provoke focus formation when cotransfected with activated Ha-ras into primary rat embryo fibroblasts (REFs). Cyclin E/Ha-ras transformed cells are highly tumorigenic in synergeneic rats, are able to form colonies in soft agar and show protection towards apoptosis upon serum starvation or DNA damage compared to cells transformed by the combination of Myc, cyclin D1 or SV40 large T-antigen and Ha-ras. Lines that were established after cyclin E/Ha-ras or cyclin D1/Ha-ras transformation contain a large percentage of polyploid cells. This was not observed in cells transformed with other oncoproteins and Ha-ras pointing to an involvement of D- and E type cyclins in genomic instability. The cyclin dependent kinase inhibitors p21 and p27 but also p16 completely abrogate focus formation by cyclin E and Ha-ras suggesting that the oncogenic activity of cyclin E still requires functional G1 specific cyclin/CDK complexes. Moreover, inhibition of Myc function also blocks the oncogenic activity of cyclin E indicating a requirement of Myc for cyclin E function. The findings presented here demonstrate that cyclin E can act as an oncoprotein with a potential involvement in genomic instability and the prevention of cell death. Our data also present more evidence for a strict functional interdependency between G1 cyclin/CDK complexes and c-Myc. More... »

PAGES

2615

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1201434

DOI

http://dx.doi.org/10.1038/sj.onc.1201434

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1041136918

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9399649


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