Research ArticleCancer

The p130 Isoform of Angiomotin Is Required for Yap-Mediated Hepatic Epithelial Cell Proliferation and Tumorigenesis

See allHide authors and affiliations

Science Signaling  03 Sep 2013:
Vol. 6, Issue 291, pp. ra77
DOI: 10.1126/scisignal.2004060

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Oncogenic Times 2

Proteins in the angiomotin (Amot) family can either promote or inhibit tumorigenesis through their actions on the Hippo-Yap pathway. Yi et al. found that the p130 isoform of Amot enhanced the activity of the transcription factor Yap to promote liver tumorigenesis. Mice with a liver-specific deficiency in Amot exhibited normal liver development but had reduced incidence of liver tumors in two models of hepatic cancer. By binding Yap and inhibiting its phosphorylation, Amot-p130 increased the nuclear translocation of Yap. In the nucleus, Amot-p130 enhanced the transcriptional activity of Yap for a subset of target genes, including those associated with tumorigenesis. Thus, the p130 isoform of Amot performs dual oncogenic functions by promoting Yap nuclear translocation and augmenting the activity of Yap at cancer-associated genes.

View Full Text

Stay Connected to Science Signaling