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Analyses were performed with SAS software (version 9.2; SAS Institute). All P values were 2 tailed, with the significance level set at P?.05.By increasing intracellular cGMP levels, sildenafil could deregulate diverse physiological functions, such as phototransduction, vascular permeability, proliferation, and apoptosis.33 Cancer metastasis requires invasion in multiple steps and cellular adhesion to vasculature or anoikis resistance.34 Therefore, sildenafil could induce cell invasion by fostering other cellular abilities. The Braf-V600E mutation has been shown to induce both melanocyte senescence and melanoma in vivo.10 Whether PDE5A inhibition may help promote or escape melanocyte senescence in laboratory experiments is unknown, particularly in BRAF-driven melanomas. The finding that PDE5A down-regulation leads to increased invasion in a BRAF-specific manner may highlight the “oncogene addiction” that prevails in BRAF-mutated melanomas.8 The lack of response of RAS-mutated melanomas to sildenafil in invasion assays may be due to the complexity of RAS signaling8 because RAS activates other pathways except mitogen-activated protein kinase.35 Arozarena et al8 provided limited data on proliferation and other features of melanoma carcinogenesis, which require functional studies to clarify.
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