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Gene of the month
Gene of the month: PIK3CA
  1. K Lai1,2,3,4,5,
  2. M C Killingsworth2,4,5,
  3. C S Lee1,2,5,6
  1. 1 Ingham Institute for Applied Medical Research, Sydney, New South Wales, Australia
  2. 2 Discipline of Pathology and Molecular Medicine Research Group, School of Medicine, University of Western Sydney, Sydney, New South Wales, Australia
  3. 3 Department of Pathology, University of Sydney, Sydney, New South Wales, Australia
  4. 4 Electron Microscopy Laboratory, Liverpool Hospital, Sydney, New South Wales, Australia
  5. 5 Department of Anatomical Pathology, Liverpool Hospital, Sydney, New South Wales, Australia
  6. 6 Cancer Pathology, Bosch Institute, University of Sydney, Sydney, New South Wales, Australia
  1. Correspondence to K Lai, Discipline of Pathology and Molecular Medicine Research Group, School of Medicine, University of Western Sydney, Liverpool, NSW 2170, Australia; ken.lai{at}uws.edu.au

Abstract

PIK3CA encodes the p110α catalytic subunit of phosphatidylinositol 3-kinase (PI3K) which through its role in the PI3K/Akt pathway is important for the regulation of important cellular functions such as proliferation, metabolism and protein synthesis, angiogenesis and apoptosis. Mutations in PIK3CA are known to be involved in a wide range of human cancers and mutant PIK3CA is thought to act as an oncogene. The specific PIK3CA inhibitor, NVP-BYL719, has displayed promising results in cancer therapy and is currently under clinical trials. Furthermore, PI3K regulates autophagy, a cellular process that recycles proteins and organelles through lysosomal degradation and has recently been recognised as an attractive therapeutic target due to its pro- and anti-cancer properties. Several studies have attempted to investigate the effects of combining the inhibition of both PI3K and autophagy in cancer therapy, and an in vivo model has demonstrated that the combined use of a concomitant PI3K and autophagy inhibitor induced apoptosis in glioma cells.

  • CANCER
  • CANCER GENETICS
  • CANCER RESEARCH

https://doi.org/10.1136/jclinpath-2015-202885

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