Fig. 1
Concurrent upregulation of FoxM1 and PLK1 is correlated with poor survival of LUAD patients. a Analysis of Spearman’s coefficient for the correlations between cell cycle-regulatory factors including PLK1, FOXM1, CCNA1, CCNB1, CCND1, CCNE1, CDK1, CDK2, PCNA, and MKI67. b-d The overall survival (OS) of patients with non-small lung cancer (n = 1885) (b), lung adenocarcinoma (LUAD) (n = 703) (c), and stages 3–4 of LUAD (n = 137) (d) were analyzed according to PLK1 and FOXM1 expression levels using KM PLOTTER. High (Hi) and low (Lo) were generated by separating patients according to expression at the median cut-off. e Using human lung tissues from LUAD patients and normal individual, immunohistochemistry analysis was displayed with anti-FoxM1 (Green) and anti-p-Serinie (Red) antibodies. The relative intensity of cells that exhibited positive FoxM1 was analyzed and plotted. WD, well differentiated (grade 1); MD, moderately differentiated (grade 2); PD, poorly differentiated (Grade 3), n > 5000. *p < 0.05; **p < 0.01; ***p < 0.001. Data are presented as mean ± SD. f and g A549, NCI-H358 (H358), and NCI-H460 (H460) NSCLC cells treated with 5 ng/mL of TGF-β for 48 h. f Immunoblotting was performed to measure the expression and phosphorylation of PLK1 using specific antibodies for FoxM1, PLK1, p-PLK1T210, p-Smad2S465/S467, Smad2, E-cadherin, N-cadherin, vimentin, SNAI1, SNAI2, and β-actin in A549, NCI-H358 (H358), and NCI-H460 (H460) cells (left panel). The relative band intensities for FoxM1, p-PLK1T210, PLK1, p-Smad2.S465/S467, Smad2, E-cadherin, N-cadherin, vimentin, SNAI1, and SNAI2 were quantified using LI-COR Odyssey software (right panel). g qRT-PCR was performed for CDH1, CDH2, FOXM1, PLK1, SNAI1, SNAI2, ZEB1, and TWIST expression in A549 (left panel), NCI-H358 (middle panel), and NCI-H460 (right panel) cells. Data are presented as mean ± SD of at least three independent experiments (significantly different from the experimental control). *p < 0.05; **p < 0.01; ***p < 0.001