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14-3-3γ induces oncogenic transformation by stimulating map kinase and pi3k signaling14-3-3γ诱发致癌转换通过刺激map激酶和pi3k信号
14-3-3c Induces Oncogenic Transformation by
Stimulating MAP Kinase and PI3K Signaling
1 1,2
Vijayababu M. Radhakrishnan , Jesse D. Martinez *
1 Arizona Cancer Center, University of Arizona, Tucson, Arizona, United States of America, 2 Department of Cell Biology and Anatomy, Arizona Cancer Center, University of
Arizona, Tucson, Arizona, United States of America
Abstract
The 14-3-3 proteins are a set of highly conserved scaffolding proteins that have been implicated in the regulation of a
variety of important cellular processes such as the cell cycle, apoptosis and mitogenic signaling. Recent evidence indicates
that the expression of some of the family members is elevated in human cancers suggesting that they may play a role in
tumorigenesis. In the present study, the oncogenic potential of 14-3-3c was shown by focus formation and tumor formation
in SCID mice using 14-3-3c transfected NIH3T3 mouse fibroblast cells. In contrast, 14-3-3s, a putative tumor suppressor,
inhibited NIH3T3 transformation by H-ras and c-myc. We also report that activation of both MAP kinase and PI3K signaling
pathways are essential for transformation by 14-3-3c. In addition, we found that 14-3-3c interacts with phosphatidylinositol
3-kinase (PI3K) and TSC2 proteins indicating that it could stimulate PI3K signaling by acting at two points in the signaling
pathway. Overall, our studies establish 14-3-3c as an oncogene and implicate MAPK and PI3K signaling as important for 14-
3-3c induced transformation.
Citation: Radhakrishnan VM, Martinez JD (2010) 14-3-3c Induces Oncogenic Transformation by Stimulating MAP Kinase and PI3K Signaling. PLoS ONE 5(7):
e11433. doi:10.1371/journal.pone.0011433
Editor: Mikhail V. Blagosklonny, Roswell Park Cancer Institute, United Stat
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