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. 2017 Apr 21;8(34):56051–56065. doi: 10.18632/oncotarget.17359

Figure 4. Decreased phosphatidylinositol (PI) and increased INPP5K expression result in decreased activation of AKT and increased expression of AR in CPT1A KD cells.

Figure 4

A. Increased mRNA of INPP5K (inositol phosphatase, *p < 0.01) in LNCaP CPT1A KD cells. B. Phospholipid analysis of the CPT1AKD cells. The x-axis represents phosphatidic acid, phosphatidylcholine, phosphatidylethanolamine, phosphatidylglycerol, phosphatidylinositol and phosphatidylserine, respectively. The graph represents the sum of the area ratios of every molecular species in each phospholipid class, normalized to the total phospholipid content in each extract of cells, and it shows decreased total abundance of PI species and increased PC species (*p ≤ 0.05 compared to NT control). The inset represents the area ratio of specific PI(18:0/20:4) species (*p < 0.05 compared to NT control). C. Representative array blot (Cell Signaling) of CPT1A-KD cells showing decreased p-AKT signal. D. Signal array quantification, *p < 0.001 compared to control (NT clones). E.-F. Representative western blots showing CPT1A-KD and double CPT1A+INPP5K KD cell lysates probed for p-AKT, INPP5K, CPT1A and AR in the double KD cell lysates. G. Diagram of the site of action of INPP5K, PI and its potential effect on AR expression via decreased activation of p-AKT. The decreased expression of CPT1A (1) leads to increased phospholipid degradation and increased INPP5K phosphatase activity, (2) resulting in decreased AKT expression and activation (3). This consequent decrease in p-AKT leads to increased AR protein expression and action, increasing PSA (KLK3) and resulting in a more differentiated phenotype.