Journal
CANCER CELL
Volume 16, Issue 2, Pages 115-125Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2009.06.006
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Funding
- NIGMS NIH HHS [R01 GM041890-23, R01 GM041890] Funding Source: Medline
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We report that knocking down the expression of inositol polyphosphate 4-phosphatase type II (INPP4B) in human epithelial cells, like knockdown of PTEN, resulted in enhanced Akt activation and anchorage-independent growth and enhanced overall motility. In xenograft experiments, overexpression of INPP4B resulted in reduced tumor growth. INPP4B preferentially hydrolyzes phosphatidylinositol-3,4-bisphosphate (PI(3,4)P-2) with no effect on phosphatidylinositol-3.4.5-triphosphate (PI(3,4,5)P-3), suggesting that PI(3,4)P-2 and PI(3,4,5)P-3 may cooperate in Akt activation and cell transformation. Dual knockdown of INPP4B and PTEN resulted in cellular senescence. Finally, we found loss of heterozygosity (LOH) at the INPP4B locus in a majority of basal-like breast cancers, as well as in a significant fraction of ovarian cancers, which correlated with lower overall patient survival, suggesting that INPP4B is a tumor suppressor.
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