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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: Cancer J. 2013 May-Jun;19(3):238–246. doi: 10.1097/PPO.0b013e31829a68eb

Figure 1. Phospholipase A signaling in response to ionizing radiation.

Figure 1

Ionizing radiation activates cytosolic phospholipase A2 (cPLA2) which cleaves phosphatidylcholine (PC) to yield lysophosphatidylcholine (LPC). LPC can phosphorylate Akt and ERK1/2. This activation leads to increased vasculature and enhanced tumorogenesis and invasion leading to radioresistance of the tumor. LPC is a secondary messenger to many signaling pathways that stimulate endothelial survival and proliferation by regulating the cytokine synthesis, endothelial growth factor expression and chemotaxis. Autotaxin that posses the lysophospholipase D (LysoPLD) activity catalyzes the reaction by cleaving the headgroup of LPC to form lysophosphatidic acid (LPA). LPA can then bind to lysophosphatidic acid receptors (LPA1–3). LPA1–3 belongs to the Endothelial differentiation gene family (EGD). LPA1 is highly expressed in the nervous system and is required for development of the brain. LPA2 is highly expressed in immune system organs such as the thymus and spleen. LPA3 is highly expressed in reproductive organs such as the testis and uterus and is linked with ovarian cancers.