Fig. 2: Knockdown KLF7 inhibits the stemness and migration of OSCC.
From: KLF7-regulated ITGA2 as a therapeutic target for inhibiting oral cancer stem cells

A Immunoblot assay of KLF7, NANOG, VIM, and e-cad protein levels in CAL27 and HSC3 cells after stable silencing KLF7. WT wild type, NC Negative control, VIM Vimentin, E-cad E-cadherin. B In vivo limiting dilution assays were performed using control cells and KLF7-silenced CAL27 cells, and the frequency of allograft formation at each injected cell dose was determined and is presented (n = 5 per group). The data were analyzed using ELDA software. C Diameter and number of spheres formed by CAL27 cells and HSC3 cells after stable silencing KLF7; data are presented as mean ± SD from five independent experiments, statistical significance was determined using Student’s t-test. Scale bar, 100 μm. D The proportion of CD133+ and ALDH+ cells in CAL27 cells and HSC3 cells after stable silencing KLF7; data are presented as mean ± SD from three independent experiments, statistical significance was determined using Student’s t-test. E Immunoblot assay of KLF7, Nanog, Vim, and E-cad protein levels in CAL27 and HSC3 cells after stable overexpression of KLF7. EV empty vector, oe overexpress. F The proportion of CD133+ and ALDH+ cells in CAL27 cells and HSC3 cells after stable overexpression of KLF7; data are presented as mean ± SD from three independent experiments, statistical significance was determined using Student’s t-test. G Diameter and number of spheres formed by CAL27 cells and HSC3 cells after stable silencing KLF7; data are presented as mean ± SD from five independent experiments, statistical significance was determined using Student’s t-test. Scale bar, 100 μm.