Oncogenic Ras-driven cancer

Campbell and Der 2004). AKT, in turn, has been shown to activate eNOS through phosphorylation of SI 177 in endothelial cells. We thus tested whether eNOS is phosphorylated and thereby activated at the AKT site SI 177 in the cancer most characterized by oncogenic Ras mutations, human pancreatic cancer (Bos 1989). A panel of nine pancreatic cancer cell lines and two normal pancreatic tissue specimens were immunoblotted with an a-phospho(S 1177)-eNOS antibody (Chen et al. 1999 Michell et al. 1999), with the finding that S1177 phosphorylation of eNOS was elevated in a subset of the mmor cell lines samples compared to the normal tissue control (Fig. 2.2a and (Lim et al. 2008)). We extended these results to acmal pancreatic cancer tumor specimens, only this time finding an increase in SI 177 phosphorylation in all tumor samples compared to the matched and unmatched normal controls (Fig. 2.2b and (Lim et al. 2008)). eNOS is thus phosphorylated at the AKT site SI 177 in Ras-driven human pancreatic cancer specimens. 

Blasco, R. B., Francoz, S., Santamaria, D., Canamero, M., Dubus, P, Charron, J., Baccarini, M., and Barbacid, M. (2011). c-Raf, but not B-Raf, is essential for development of K-Ras oncogene-driven non-small cell lung carcinoma. Cancer Cell 19, 652-663. 

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