Phosphoinositide 3-Kinase Regulates Glycolysis through Mobilization of Aldolase from the Actin Cytoskeleton Academic Article uri icon


MeSH Major

  • Fructose-Bisphosphate Aldolase
  • Phosphatidylinositol 3-Kinases


  • The phosphoinositide 3-kinase (PI3K) pathway regulates multiple steps in glucose metabolism and also cytoskeletal functions, such as cell movement and attachment. Here, we show that PI3K directly coordinates glycolysis with cytoskeletal dynamics in an AKT-independent manner. Growth factors or insulin stimulate the PI3K-dependent activation of Rac, leading to disruption of the actin cytoskeleton, release of filamentous actin-bound aldolase A, and an increase in aldolase activity. Consistently, PI3K inhibitors, but not AKT, SGK, or mTOR inhibitors, cause a significant decrease in glycolysis at the step catalyzed by aldolase, while activating PIK3CA mutations have the opposite effect. These results point toward a master regulatory function of PI3K that integrates an epithelial cell's metabolism and its form, shape, and function, coordinating glycolysis¬†with the energy-intensive dynamics of actin remodeling.

publication date

  • January 28, 2016



  • Academic Article



  • eng

PubMed Central ID

  • PMC4898774

Digital Object Identifier (DOI)

  • 10.1016/j.cell.2015.12.042

PubMed ID

  • 26824656

Additional Document Info

start page

  • 433

end page

  • 46


  • 164


  • 3