Skip to main content
. 2021 Jul 27;40(37):5613–5625. doi: 10.1038/s41388-021-01961-9

Fig. 2. B-Myb enhances colorectal cancer cell proliferation.

Fig. 2

a Lentivirus-mediated stable B-Myb overexpression. HCT116 and RKO cells were infected with the empty control and B-Myb-expressing lentiviral particles, and then selected in the presence of puromycin to obtain the control (LV-control) and B-Myb overexpression (LV-B-Myb) stable cells. Expression of B-Myb was examined by qRT-PCR and immunoblot analysis. b Lentivirus-mediated stable B-Myb knockdown. HCT116 and RKO cells were infected with the lentiviral particles expressing negative control shRNA and B-Myb shRNA, and then selected in the presence of puromycin to generate the polyclonal control (shNC) and B-Myb knockdown (shB-Myb) stable cells. Expression of B-Myb was examined by qRT-PCR and immunoblot analysis. c, d B-Myb increases cell proliferation. Cell proliferation was detected by CCK8 assay in the stable B-Myb overexpression or knockdown cells at the indicated time points. e, f B-Myb increases colony formation. Cells were seeded on plastic plates for plate clone formation assay. Representative images were shown. g, h B-Myb promotes colorectal cancer growth in vivo. Stable B-Myb overexpression or knockdown HCT116 cells were injected subcutaneously into the dorsal flanks of nude mice. The tumor size was measured 1–2 times a week for tumor growth curve construction. The tumor weight was measured at the end of the experiment. Data represent the mean ± SD. All experiments were performed in triplicates. *p < 0.05, **p < 0.005, ***p < 0.001.