Research Paper Volume 12, Issue 8 pp 6904—6927

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

Figure 2. UAP1L1 knockdown inhibited gastric cancer development in vitro. (A, B) Cell models with or without UAP1L1 knockdown were constructed by transfecting shUAP1L1 or shCtrl. The knockdown efficiency of UAP1L1 in BGC-823 and SGC-7901 cells was assessed by qPCR (A) and western blotting (B). (C) MTT assay was employed to show the effects of UAP1L1 on cell proliferation of BGC-823 and SGC-7901 cells. (D) Flow cytometry was performed to detect cell apoptosis of BGC-823 and SGC-7901 cells with or without UAP1L1 knockdown. (E) Human Apoptosis Antibody Array was utilized to analyze the regulatory ability of UAP1L1 on expression of apoptosis-related proteins in SGC-7901 cells. (F) Cell cycle distribution was estimated in BGC-823 and SGC-7901 cells with or without UAP1L1 knockdown. (G) The effects of UAP1L1 on cell migration ability of BGC-823 and SGC-7901 cells were evaluated by wound-healing assay. (H) The expression of EMT-related proteins including Snail, N-cadherin and Vimentin was detected by western blotting in BGC-823 and SGC-7901 cells of shUAP1L1 and shCtrl groups. 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.