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Targeting PI3K:
The shutdown of cell survival signaling

PI3K

The phosphatidylinositol 3-kinase (PI3K) pathway is critical for cell survival and cell growth, and can be activated by growth factors binding to cell surface receptors. It is an intricate signaling cascade that is among the most frequently activated pathways in cancer. PI3K is the subject of extensive research at Genentech, a member of the Roche Group.

Targeting PI3K
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PI3K is composed of a catalytic subunit that confers enzyme activity, and a regulatory subunit, which binds to cell surface receptors and to the Ras protein. The p110 alpha catalytic subunit of PI3K, as well as the Phosphatase and Tensin homolog tumor suppressor, PTEN, a negative regulator of this pathway, are commonly mutated in a wide range of human tumors.1 Additionally, many cell surface receptors that activate PI3K are subject to being mutated or amplified in tumors.1 Dysregulation of the PI3K pathway is a key step in tumorigenesis as PI3K signaling can affect many cellular processes.1

Abnormal PI3K signaling may lead to1

  • Abnormal cell growth
  • Increased/uncontrolled proliferation
  • Increased cell survival
  • Enhanced cancer cell motility

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Reference:
1.
Knight ZA, Shokat KM. Chemically targeting the PI3K family. Biochem Soc Trans. 2007;35:245-249. PMID: 17371250