Figure 3.
CES2 represses OSCC cell progression in vitro and in vivo. CAL33 and UM1 cells stably overexpressing the empty vector or CES2 and HSC3 and CAL27 cells with the negative control (NC) or transiently silenced CES2 (si-1 and si-2) were used to study the biological function of CES2. (A–D) The transfection efficiencies of the vector and CES2 plasmids and siRNA effects (NC, si-1 and si-2) were examined by qPCR and western blot assays, respectively. The relative mRNA (A, C) and protein (B, D) levels of CES2. β-Actin was used as the endogenous control. (E, F) The relative proliferation rates of stable empty vector- or CES2-overexpressed cells were measured by CCK-8 assays (E), and the relative proliferation rates of these cells were measured in cells with the NC or transiently silenced CES2 (si-1 and si-2) (F). (G–J) Migratory and invasive abilities were detected with Transwell assays without (G, H) and with Matrigel (I, J), respectively, in stably empty vector- or CES2- overexpressing cells and in cells with the NC or CES2 transiently silenced (si-1 and si-2). (K–M) Representative images of tumor nodules (K), quantification of tumor volumes (L) and weights (M) in mouse xenografts. The mean ± s.d.; ∗, P < 0.05; Student’s t tests.