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. 2012 Apr 1;11(7):1383–1392. doi: 10.4161/cc.19800

Figure 4.

Figure 4

Fatty acid oxidation regulates the secretory state of Ras-induced senescence. (A) Expression of CPT1A in control-infected or Ras-infected cells following knockdown with a control vector (−) or one of two independent shRNAs directed at CPT1A. (B) Knockdown of CPT1A reduces oxygen consumption in Ras-infected cells, consistent with the role of increased fatty acid oxidation in OIS cells. (C) Knockdown of CPT1A does not alter Ras-mediated growth arrest. (D) CPT1A knockdown does not alter Ras-induced activation of the DDR as assessed by γH2AX staining. The percentage of cells with positive nuclei foci is shown in white. (E) Relative levels of cytokine secretion in Ras-infected cells treated with vehicle (filled bars) or for six hours with the CPT1 inhibitor Etomoxir (open bars). (F) Normalized levels of secreted cytokines in Ras-infected cells with a scrambled control shRNA (filled bar) or Ras-infected cells using either of two different shRNAs directed at CPT1A (single and double hatched bars). n > 3 replicates per condition for all experiments, *p < 0.05 and **p < 0.01.