Journal Article

Role of the β isoform of 14-3-3 proteins in cellular proliferation and oncogenic transformation

Yoshihiro Takihara, Yoshiko Matsuda and Junichi Hara

in Carcinogenesis

Volume 21, issue 11, pages 2073-2077
Published in print November 2000 | ISSN: 0143-3334
Published online November 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.11.2073
Role of the β isoform of 14-3-3 proteins in cellular proliferation and oncogenic transformation

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The 14-3-3 proteins are associated with proto-oncogene and oncogene products. Here, we generated NIH 3T3 cells overexpressing the β isoform of the 14-3-3 proteins (14-3-3 β) to examine the function of this isoform in cellular proliferation and oncogenic transformation. Overexpression of 14-3-3 β in NIH 3T3 cells stimulated cell growth and supported anchorage-independent growth in soft agar medium and tumor formation in nude mice. To elucidate the molecular mechanisms of 14-3-3 β-mediated NIH 3T3 transformation, we examined the activity of mitogen-activated protein kinase (MAPK) after serum stimulation. Overexpression of 14-3-3 β augmented MAPK activity after serum stimulation, and MAPK activity correlated well with the amount of 14-3-3 β expression. The colony-forming ability of NIH 3T3 cells overexpressing 14-3-3 β in soft agar medium was efficiently abolished by exogenous expression of a dominant-negative mutant of MEK1 and 14-3-3 β physically interacted with Raf-1 in these cells. These findings indicate that 14-3-3 β has oncogenic potential, mainly through enhancement of Raf-1 activation and resultant augmentation of signaling in the MAPK cascade.

Keywords: MAPK, mitogen-activating kinase; PKC, protein kinase C; RA, retinoic acid.

Journal Article.  4249 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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