Figure 6 | British Journal of Cancer

Figure 6

From: PLD1 is overexpressed in an ER-negative MCF-7 cell line variant and a subset of phospho-Akt-negative breast carcinomas

Figure 6

Model of alternative mammalian target of rapamycin (mTOR) Activation by PLD1 in breast cancer. Receptor tyrosine kinases (RTKs) activate several downstream signals including small GTPases, PKCα, and PI3K. Phospholipase D1 (PLD1) is activated, by either members of the small GTPase family or by PKCα, and is dependent on phosphatidylinositol-4,5-bis-phosphate (PIP2) to generate phosphatidic acid (PA), whereas Akt requires PIP3 for localisation to the plasma membrane and activation. Phosphatidic acid or phosphorylated Akt activates the protein kinase mTOR, which phosphorylates its downstream effectors p70S6K and 4E-BP1, thereby promoting cell growth and proliferation (adapted from Foster and Xu, 2003).

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