Atrial natriuretic peptide modulates the proliferation of human gastric cancer cells via KCNQ1 expression.

摘要: Atrial natriuretic peptide (ANP) and brain NP (BNP) belong to the family that regulates mammalian blood volume pressure. ANP signaling through receptor A (NPR-A)/cyclic guanosine 3′5′-monophosphate (cGMP)/ cGMP-dependent protein kinase (PKG) activates various downstream effectors involved in cell growth, apoptosis, proliferation inflammation. Evidence has shown critical role of plasma K+ channels regulation tumor proliferation. However, gastric cancer cells is not clear. In present study, expression NPR-A human line, AGS, effect on AGS were investigated using western blotting, immunofluorescence, qPCR patch clamp assays. The current was also analyzed cells. expressed line. Lower concentrations promoted cells, although higher decreased their Significant increases levels cGMP activity observed treated with 10−10, 10−9 10−8 M compared controls, but no significant differences 10−7 10−6 groups. results showed significantly increased tetraethylammonium (TEA)- 293B-sensitive current, while TEA- current. 10−10 upregulated potassium voltage-gated channel, KQT-like subfamily, member 1 (KCNQ1) at mRNA levels, downregulated KCNQ1. data indicated lower have opposite effects or -independent pathways. KCNQ1 upregulation downregulation by ANP, respectively, separate promotion inhibition