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. Author manuscript; available in PMC: 2012 Nov 1.
Published in final edited form as: Trends Pharmacol Sci. 2011 Sep 4;32(11):644–651. doi: 10.1016/j.tips.2011.07.001

Figure 1.

Figure 1

Oncogenic signaling pathways regulated by NO and PP2A. NO activates numerous signaling pathways associated with cancer cell proliferation, survival, chemoresistance and migration. Some of the molecular and pathway targets of NO signaling include sGC, HIF-1α, Src, PI3K/Akt, EGFR, Ras, c-Myc and ERK-1/2. Furthermore, NO activates oncogenic pathways by redundant mechanisms; for example, ERK-1/2 is activated from either Ras signaling or sGC activation and PI3K/Akt signaling is activated by either EGFR or Src kinases. These redundant mechanisms indicate that single agent therapies could fail to limit oncogenic NO signaling. The tumor suppressor PP2A is the endogenous negative regulator of many NO-activated signaling pathways. We propose that pharmacological activation of PP2A could represent an effective strategy to limit the myriad of pro-tumor NO effects.