Fig. 1: Inactivation of USP7 promotes cell progression of p53-deficient lung cancer H1299 cell line.
From: USP7 facilitates SMAD3 autoregulation to repress cancer progression in p53-deficient lung cancer
A Schematic of guide RNA (gRNA) design and genomic sequences of USP7 knockout (KO) clones. KO_E2 Exon 2 targeted, KO_E3 Exon 3 targeted, PAM protospacer adjacent motif. B Immunoblots of USP7 in the lysates from wildtype (WT) or indicated USP7 KO H1299 cells. β-actin is the loading control. C–F Cell proliferation (C, D) and cell cycle profiling (E, F) assays of wildtype (WT) and USP7 KO (HKO_E2 and HKO_E3) H1299 cell lines in culture media supplemented with 10% (C, E) or 1% fetal bovine serum (FBS) (D, F). Results are mean ± SD from three independent experiments. G Apoptotic cell profiling by Annexin V staining in wildtype (WT) or USP7 KO (HKO_E2) H1299 cells treated with 1% FBS for 6 days. H The growth curves of xenografted tumors of wildtype (WT) or USP7 KO (HKO_E2) H1299 cell lines. The tumor sizes were determined every 7 days using an external caliber. The data are presented as mean ± SD from a cohort of six mice. The inset showing the representative images of WT or HKO_E2 cells xenografted tumors on day 42. Student’s t-test, *p < 0.05; **p < 0.01; ***p < 0.001.
