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. 2019 May 31;9(14):4208–4220. doi: 10.7150/thno.33803

Figure 1.

Figure 1

USP5 regulates colorectal cancer cell growth. A & B. The lentivirus-delivered shRNAs against twenty DUBs and controls were constructed. HCT116 cells were infected with different lentivirus-delivered shRNAs, and cell number was counted from 0 to 5 days. The cell growth curve was made (A), and the photos were taken (B). C. HCT116 cells were stably infected with lentiviral shUSP5#1, shUSP5#2, shUSP5#3 or control, followed by immunoblotting and CCK-8 staining at day 0, 2, 4 and 6. Immunoblotting assay was also performed against USP5, Cyclin D1 and GAPDH at day 6. *p<0.01. D. HCT116 cells were transfected with plasmids expressing wild-type Myc-USP5 (Myc-USP5-WT), the catalytically inactive mutant of USP5 (Myc-USP5-C335A) or empty vector (EV), followed by CCK-8 staining at day 0, 1, 2 and 4. Immunoblotting was also performed to detect the expression levels of Myc-USP5, Cyclin D1 and GAPDH at day 4. *p<0.05, **p<0.01. E. HCT116 cells stably infected with lentiviral shUSP5#3 were subcutaneously injected into the right flank of each mouse. When tumors were palpable after seven days, tumor sizes were monitored twice a week for continuously three weeks. *p<0.05, **p<0.01. F. Tumors were excised from nude mice at the end of the experiment. G. Tumor weight was measured at the end of the experiment. H. The excised tumors were prepared for immunoblotting against USP5 and Cyclin D1. GAPDH was used as a loading control.