RÉSUMÉ
Objective:To observe the expression of long-chain noncoding RNA (lncRNA) SCAMP1-AS1 in esophageal cancer tissues, and explore the effect of SCAMP1-AS1 on the proliferation and migration of esophageal cancer cells and the possible molecular mechanism.Methods:Real-time fluorescent quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression level of SCAMP1-AS1 in 37 cases of esophageal cancer tissues and adjacent tissues surgically resected in Huangshi Central Hospital of Edong Medical Group from March 2017 to August 2020. RT-qPCR was also used to detect the expression level of SCAMP1-AS1 in 4 types of esophageal cancer cells (EC9706, TE-13, KYSE30, Eca109) and normal esophageal epithelial cells HET-1A. The cells with the lowest expression were selected, the negative control lentivirus (LV-NC) infection was used as the control group, and the recombinant lentivirus carrying SCAMP1-AS1 sequence (LV-SCAMP1-AS1) infection was used as the experimental group. RT-qPCR was used to detect the expression of SCAMP1-AS1 in esophageal cancer cells after infection. Cell counting kit 8 (CCK-8) and Transwell chamber method were used to detect the proliferation and migration ability of esophageal cancer cells. Bioinformatics methods predicted the target genes of SCAMP1-AS1, and dual luciferase reporter experiments verified the interaction of SCAMP1-AS1 with target gene. RT-qPCR detected the expression of target genes. Western blotting detected the expression of cell proliferation and migration phenotype proteins.Results:The relative expression level of SCAMP1-AS1 in esophageal cancer tissue was significantly lower than that in adjacent tissues (1.26 ± 0.48 vs. 8.03 ± 1.17, P<0.01). The relative expression levels of SCAMP1-AS1 in esophageal cancer cells EC9706, TE-13, KYSE30, Eca109 were all lower than that in normal esophageal epithelial cells (0.54 ± 0.05, 0.14 ± 0.02, 0.46 ± 0.07, 0.77 ± 0.05 vs.1.00 ± 0.06, P<0.05), and the expression of SCAMP1-AS1 in TE-13 cells was the lowest ( P<0.01). Compared with the control group, the expression of SCAMP1-AS1 in TE-13 cells in the experimental group was up-regulated ( P<0.01), the proliferation ability of the cells was reduced ( P<0.01), and the migration ability of the cells was reduced ( P<0.01). miR-483-5p was the direct target of SCAMP1-AS1. Compared with the control group, the expression of miR-483-5p was down-regulated in TE-13 cells in the experimental group ( P<0.01), and the expression of cell proliferation and migration phenotype proteins was down-regulated. Conclusions:The expression of lncRNA SCAMP1-AS1 is down-regulated in esophageal cancer. SCAMP1-AS1 can inhibit the proliferation and migration of esophageal cancer TE-13 cells by targeting the expression of miR-483-5p. SCAMP1-AS1 is expected to become a potential molecular therapeutic target for esophageal cancer.
RÉSUMÉ
Objective:To explore the influence of microRNA (miRNA)-6751-3p expression on the proliferation and migration of gastric cancer cells and its molecular mechanism.Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of miR-6751-3p in gastric cancer cell lines (MGC803, BGC823, SGC7901, HS-746T) and normal gastric mucosal epithelial cells (GES-1). The gastric cancer cell lines with the lowest expression level of miR-6751-3p were divided into control group and experimental group, and were transfected with miR-NC and miR-6751-3p mimics respectively. qRT-PCR detected the expression level of miR-6751-3p in the two groups of cells. CCK-8 method and scratch healing test were used to detect the proliferation and migration of miR-6751-3p overexpressing cells. The potential target genes of miR-6751-3p were predicted through Deepbase v2.0 and microRNA.org online websites, and the dual luciferase reporter gene experiment was used to verify. qRT-PCR and Western blot were used to detect the expression of target genes in miR-6751-3p overexpression cells.Results:Compared with normal gastric mucosal epithelial cells, the expression of miR-6751-3p was significantly down-regulated in gastric cancer cell lines ( P<0.05), and the cell line with the lowest expression level was MGC803 cells ( P<0.01). Compared with the control group, overexpression of miR-6751-3p can inhibit the proliferation ability ( P<0.05). The scratch healing rate of MGC803 cells in the control group and the experimental group were (65.14±5.65)% and (23.40±6.78)%, respectively. Compared with the control group, the scratch healing rate of MGC803 cells in the experimental group was significantly lower ( t=4.73, P<0.01). The online website predicts that the target gene of miR-6751-3p may be fatty acid binding protein 5 ( FABP5), and miR-6751-3p can complementally bind FABP5 messenger RNA (mRNA) ( t=4.01, P<0.01). Compared with the control group, overexpression of miR-6751-3p can inhibit the expression of FABP5 gene in MGC803 cells ( P<0.01). Conclusion:The expression of miR-6751-3p in gastric cancer cell lines is low, and the overexpression of miR-6751-3p can inhibit the proliferation and migration of gastric cancer MGC803 cells by down-regulating the FABP5 gene.