Effects of LncRNA SNHG25 on Proliferation and Migration of Bladder Cancer Cells by Regulating miR-6838-5p/FOXK1 Axis
ZHANG Shuangyang, YAO Jun, CHEN Chen, DENG Jiyi, SUN Chengliang*
This study aims to investigate the effect of LncRNA SNHG25 (long con-conding RNA small nucleolar RNA host gene 25) regulating the miR-6838-5p/FOXK1 (microRNA-6838-5p/forkhead box K1) axis on the proliferation and migration of bladder cancer cells. QRT-PCR was used to measure the expression of LncRNA SNHG25, miR-6838-5p, and FOXK1 mRNA in tissues and cells. T24 cells were grouped into NC (negative control) group, LncRNA SNHG25 knockdown negative control (si-NC) group, LncRNA SNHG25 knockdown (si-SNHG25) group, si-SNHG25+miR-6838-5p inhibitor (si-SNHG25+in-miR-6838-5p) group and si-SNHG25+FOXK1 overexpression (si-SNHG25+oe-FOXK1) group. QRT-PCR was used to measure the trans fection efficiency of T24 cells in each group. CCK-8 method, BrdU method, colony formation assay, scratch as say, and Transwell assay were used to detect cell proliferation and migration. Western blot was used to measure the levels of p53, FOXK1, Survivin, MMP9, Twist1, and SOX9 proteins in T24 cells. The luciferase reporter gene and RIP were used to measure the interaction between LncRNA SNHG25 and miR-6838-5p, and between miR-6838-5p and FOXK1. In vivo experiments were used to detect the effect of LncRNA SNHG25 on tumor growth. LncRNA SNHG25 and FOXK1 mRNA levels were up-regulated and miR-6838-5p was down-regulated in bladder cancer tissues or cells (T24, 5637 and EJ) (P<0.05). Compared with the si-NC group, the si-SNHG25 group had lower LncRNA SNHG25, cell viability, BrdU positive rate, colony formation, wound healing rate, number of migrating cells, MMP9, Twist1, SOX9, FOXK1, and Survivin in T24 cells, and higher miR-6838 5p and p53 (P<0.05). Compared with the si-SNHG25 group, the si-SNHG25+in-miR-6838-5p group and si SNHG25+oe-FOXK1 group had lower viability, BrdU positive rate, colony formation number, wound healing rate, number of migrating cells, MMP9, Twist1, SOX9, FOXK1, and Survivin in T24 cells, and higher p53 (P<0.05). The result showed that LncRNA SNHG25 had a targeted relationship with miR-6838-5p, and miR 6838-5p had a targeted relationship with FOXK1. And all All three components showed significant enrichment in Ago2 complexes (P<0.05). Knocking down LncRNA SNHG25 reduced tumor tissue volume and mass in vivo, downregulated LncRNA SNHG25 and FOXK1 mRNA levels, and upregulated miR-6838-5p (P<0.05). Knock down of LncRNA SNHG25 suppresses the proliferation and migration of bladder cancer cells through the miR 6838-5p/FOXK1 signaling axis.
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