Skip to main content
Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: The role of TRPV1 ion channels in the suppression of gastric cancer development

Fig. 7

TRPV1/Ca2+-mediated GC suppression through activation of CaMKKβ/AMPK phosphorylation. a Representative time course of 5 mM CaCl2-induced [Ca2+]i signaling in TRPV1-overexpressed BGC823 cells (middle) vs. NC (left) and TRPV1-overexpressed BGC823 cells treated with SB-705498 (50 μM) (right). Summary data are shown as a bar graph (**P < 0.01, ****P < 0.0001, n = 20 cells). b Representative time course of 5 mM CaCl2-induced [Ca2+]i signaling in TRPV1-knockeddown MKN45 cells (middle) vs. NC (left). Summary data are shown as a bar graph (right) (***P < 0.001 vs. NC, n = 20 cells). c Expression levels of CaMKKβ proteins after TRPV1 overexpression in BGC823 cells or TRPV1 knockdown in MKN45 cells. Representative images are shown on the left and summary data on the right (*P < 0.05 vs. NC, n = 3). d Effects of CaMKKβ knockdown on CaMKKβ expression in TRPV1-overexpressed BGC823 or NC cells (*P < 0.05, n = 3). e Effects of BAPTA-AM (2 μM) on CaMKKβ expression in TRPV1-overexpressed BGC823 or NC cells (*P < 0.05, n = 3). f Effects of CaMKKβ knockdown on AMPK phosphorylation in TRPV1-overexpressed BGC823cells or NC cells (*P < 0.05, **P < 0.01, n = 3). g Proposed mechanisms of TRPV1-mediated GC suppression. The Ca2+ entry through TRPV1 channels causes CaMKKβ activation and AMPK phosphorylation that inhibits cyclin D1 and MMP2, leading to suppression of GC cell proliferation, migration and invasion. OE: overexpression, KD: knockdown, CaMKKβ: calcium/calmodulin-dependent protein kinase kinase β, AMPK: adenosine mono phosphate activated protein kinase, MMP2: matrix metalloproteinase-2

Back to article page
\