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. 2020 Jan 10;14(2):387–406. doi: 10.1002/1878-0261.12626

Figure 2.

Figure 2

SNX16 promotes CRC cells growth in vitro. (A, B) Effects of SNX16 knockdown and overexpression were analyzed by qRT‐PCR and western blot analysis. GAPDH was used as the loading control. **P < 0.01, ***P < 0.001. (C). Knockdown of SNX16 inhibited HT29 and LoVo cell proliferation, whereas ectopic expression of SNX16 promoted SW480 cell proliferation, as determined by the MTT assay. The results are shown as the means ± SEMs (n = 5), ****P < 0.0001. (D) The effect of knockdown or overexpression of SNX16 on CRC cell proliferation capacity was analyzed by the EdU assay. The results are shown as the means ± SEMs (n = 5), *P < 0.05, **P < 0.01. (E) Effect of SNX16 on colony formation by CRC cells. The results are shown as means ± SEMs (n = 3), **P < 0.01, ****P < 0.0001. (F) SNX16 accelerated the G1‐S transition of the cell cycle, as indicated by flow cytometry. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. (G) SNX16 inhibited cell apoptosis, as determined by Annexin V‐APC/PI staining and flow cytometry. (H) The effect of knockdown or overexpression of SNX16 on cell cycle regulators, including p21, p18, CDK6, cyclin D1, and cyclin D3, was determined by western blotting. (I) The effect of knockdown or overexpression of SNX16 on apoptosis‐associated protein caspase‐3 was analyzed by western blotting. Tubulin was used as the loading control.