Research Paper Volume 12, Issue 8 pp 6904—6927

Identification of UAP1L1 as tumor promotor in gastric cancer through regulation of CDK6

Figure 5. Knockdown of CDK6 attenuated the effects of gastric cancer cells by UAP1L1 overexpression. (A, B) Cell models with or without UAP1L1 overexpression were constructed by transfecting Control plasmids or UAP1L1 overexpression plasmids. The overexpression efficiency of UAP1L1 in SGC-7901 cells was assessed by qPCR (A) and western blotting (B). (C) Celigo cell counting assay was employed to show the effects of UAP1L1 on cell proliferation of SGC-7901 cells. (D) Colony formation assay was used to evaluate the ability of SGC-7901 cells with or without UAP1L1 overexpression to form colonies. (E) Flow cytometry was performed to detect cell apoptosis of SGC-7901 cells with or without UAP1L1 overexpression. (F, G) The effects of UAP1L1 on cell migration ability of SGC-7901 cells were evaluated by wound-healing assay (F) and Transwell assay (G). (HL) SGC-7901 cells transfected with NC(OE+KD), UAP1L1 overexpression plasmids and simultaneous UAP1L1 overexpression plasmids and shCDK6 were subjected to the detection of cell proliferation by Celigo cell counting assay (H), colony formation (I), cell apoptosis by flow cytometry (J), cell migration by wound-healing assay (K) and cell migration by Transwell assay (L). The representative images were selected from at least 3 independent experiments. Data was shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.