Norepinephrine inhibits the migratory activity of pancreatic cancer cells.

摘要: We have shown previously that norepinephrine induces migratory activity of tumour cells from breast, colon and prostate tissue via activation beta-2 adrenergic receptors. Consequently, this effect can be inhibited pharmacologically by clinically established beta-blockers. Tumour cell migration is a prerequisite for metastasis formation, accordingly we others breast cancer patients, which take beta-blockers due to hypertension, reduced formation increased survival probability as compared patients without hypertension or using other anti-hypertensive medication. Unlike the aforementioned cells, pancreatic show upon treatment. By means our three-dimensional, collagen-based assay, investigated signal transduction pathways involved in phenomenon. found conflicting on an imbalanced two usually mediate pro-migratory types. Firstly, inhibitory results pathway causes strong increase secondary signalling molecule, cAMP. In addition, phospholipase C gamma downstream protein kinase alpha were already activated cannot further norepinephrine. hypothesize constitutive cross-talk with receptor tyrosine signalling, might also deliver explanation unusual high spontaneous cells.