Fig. 4.

Expression of active PLK1 promotes tumor growth and metastasis in mouse model, which is blocked by the treatment of volasertib. a–d A549 cells expressing phosphomimetic active T210D (TD) or inactive PBD mutant W414F/V415A (FA) PLK1 were injected intravenously into the tail-veins of 4-week-old BALB/c nude mice, and the tumorigenic and metastatic properties were evaluated after 10 weeks. a Representative lung tumors from the mouse model (left panel). The number of metastatic lung tumors was counted and plotted (right panel) (n = 5). Data presented as mean ± SD. b Immunoblotting was performed using lung tissue lysates from each mouse model. N-cadherin, E-cadherin, α-SMA, vimentin, slug, snail, PLK1, RFP, and β-actin were detected using specific antibodies. c H&E staining was performed using lung tissue from the mice. *p < 0.05; **p < 0.01; ***p < 0.001. (n = 3). Data presented as mean ± SD. d Ki-67 staining was performed using lung tissue from the mice. *p < 0.05; **p < 0.01; ***p < 0.001. (n = 3). Data presented as mean ± SD. e–f Primary A549 cells expressing phosphomimetic active TD-PLK1 were injected intravenously into the tail veins of 4-week-old BALB/c nude mice. Two weeks later, the mice received 20 mg/kg of volasertib by injection every week for 3 weeks. After 5 weeks, the anti-tumorigenic and anti-metastatic properties of volasertib were evaluated. e Representative lung tumors from the mouse model (left panel). The number of metastatic lung tumors was counted and plotted (right panel) (n ≥ 4). f H&E staining was performed using lung tissue from the mice. The relative intensity of the H&E staining was plotted. *p < 0.05; **p < 0.01; ***p < 0.001. (n = 4). Data presented as mean ± SD