Fig. 5: MAO-A activates hypoxia signaling to promote the Enz resistance.

a The mRNA levels of Glut1, N-Cadherin, Timp, and VEGF-A in EnzS1-C4-2 and EnzR1-C4-2 cells were analyzed by qPCR; (n = 3 biological independent samples). b In EnzR1-C4-2 cells, MAO-A was knocked down by shRNA. And the mRNA levels of MAO-A, Slug, VEGF-A, and HIF-1α were analyzed by qPCR (left), as well as HIF-1α and VEGF-A expression by western blot (right); (n = 3 biological independent samples for qPCR). c EnzR1-C4-2 cells were treated with/without 5 μM clorgyline, and the mRNA and protein level of MAO-A, HIF-1α, and VEGF-A were analyzed by qPCR (HIF-1α and MAO-A, left) and western blot (HIF-1α and VEGF-A, right); (n = 3 biological independent samples for qPCR). d MAO-A was overexpressed (oeMAO-A) in EnzS1-C4-2 cells, and the mRNA and protein levels of MAO-A, HIF-1α, and VEGF-A were analyzed by qPCR (left) and western blot (right); (n = 3 biological independent samples for qPCR). e HIF-1α was knocked down (shHIF-1α) in EnzR1-C4-2 cells, and then the cells were treated with/without Enz. The cell viability was analyzed by MTT assay; (n = 3 biological independent samples). Data represent the mean ± SEM, error bars represent SEM. p-value was determined by two-tailed paired t-test.