Aspirin inhibits cell viability and mTOR downstream signaling in gastroenteropancreatic and bronchopulmonary neuroendocrine tumor cells

Figure 6 The effect of aspirin on GSK3 and ERK1/2 signaling in neuroendocrine BON1, NCI-H727 and GOT1 tumor cells. Human pancreatic neuroendocrine BON1 (A), human bronchopulmonary NCI-H727 (B) and midgut GOT1 (C) cells were treated with the indicated concentrations of aspirin for 24 and 48 h. The expression of pGSK3, GSK3, pERK1/2, ERK1/2, pCREB, CREB and a β-actin loading control was subsequently evaluated by Western blot analysis. A representative blot from 3 independently performed experiments is shown.