摘要
Aim To study the expression of microRNA(miR-34c-5p)in gastric cancer tissues and the mechanism of regulating the invasion and migration of gastric cancer cells. Methods The expression of miR-34c-5p mRNA in human gastric cancer tissues and cells was detected by quantitative real-time polymerase chain reaction(RT-qPCR). An overexpression model of miR-34c-5p was constructed in human gastric cancer cells. The transfection of lentivirus was observed under inverted fluorescence microscope, and the transfection efficiency was verified by RT-qPCR. Scratch test and Transwell assay were used to detect the effects of overexpression of miR-34c-5p on invasion and migration of gastric cancer cells. Western blot was used to detect the expression of MAP2K1, E-Cadherin and Vimentin in gastric cancer cells of each group. Dual-luciferase reporter assay was employed to detect whether MAP2K1 was a target gene of miR-34c-5p. Results The expression of miR-34c-5p mRNA in 10 human gastric cancer tissues was significantly lower than that in adjacent tissues(P<0.05). The expression of miR-34c-5p mRNA in gastric cancer HGC-27 cell was significantly lower than that in normal gastric mucosa GES-1 cell(P<0.01). Compared with blank control group and miR-34c-5p-NC group, miR-34c-5pmimics group significantly increased its miR-34c-5p mRNA expression level(P<0.05). The results of scratch test and Transwell experiment showed that overexpression of miR-34c-5p significantly inhibited the migration and invasion ability of gastric cancer cells(P<0.05, P<0.01). Western blot results showed that the protein expression levels of MAP2K1 and Vimentin significantly decreased and E-Cadherin markedly increased in gastric cancer HGC-27 cells after overexpression of miR-34c-5p(P<0.05). In addition, compared with mimic-NC+miR-34c-5p-mimics group, the lucifase activity of pmiR-MAP2K1-WT plasmid decreased(P<0.01), while the lucifase activity of pmiR-MAP2K1-MUT plasmid was not changed. Conclusions The low expression of miR-34c-5p in gastric cancer tissues and cells may inhibit the invasion and migration of gastric cancer cells through targeted regulation of MAP2K1 expression.
摘要
Objective To investigate the expression of mitogen-activated protein kinase kinase 1 (MAP2K1) in gastric cancer and its clinical significance. Methods Immunohistochemistry and Western blotting were used to detect the protein expression of MAP2K1 in gastric cancertissues and cells. The morphology and the expression position of MAP2K1 were observed by immunofluorescence. MAP2K1 mRNA expression in gastric cancer tissues was analyzed by data mining of Starbase database and Oneomine database. The correlation between MAP2K1 mRNA expression and clinicopathological features was analyzed by UALCAN database. Survival analysis was performed using Kaplan Meier-Plotter online analysis tools. GEPIA2 database mining the relationship between MAP2K1 and gastric cancer stem cell related factors and drug resistance related factors. Results Immunohistochemistry, immunofluorescence and Western blotting showed that MAP2K1 protein was highly expressed in gastric cancer tissues and cells, and MAP2K1 was expressed in the cytoplasm of gastric cancer. According to the analysis of various databases, the expression of MAP2K1 mRNA in gastric cancer tissue was higher than that in normal gastric tissue, and the expression of MAP2K1 mRNA was closely related to gastric cancer stage, grade, lymph node metastasis and patient gender, and the overall survival rate of gastric cancer patients in the group with high MAP2K1 mRNA expression was significantly lower than that in the group with low MAP2K1 mRNA expression, which may be related to the characteristics of gastric cancer stem cells and drug resistance. Conclusion MAP2K1 is highly expressed in gastric cancer, and its expression level may affect the poor prognosis of patients by regulating stem cell related factors and drug resistance related factors. MAP2K1 may be a new diagnostic marker to determine the prognosis of gastric cancer patients.
摘要
<p><b>BACKGROUND AND OBJECTIVE</b>Sapylin is one of the biological response modifiers. It has been used in the comprehensive treatment for advanced cancer, and its clinical efficacy has been proved. This study was to evaluate the effect of preoperative intraperitoneal injection of Sapylin in treatment of advanced gastric cancer.</p><p><b>METHODS</b>Seventy-nine patients eligible for radical gastrectomy were randomly divided into the treatment group (Sapylin + mitomycin C, 40 patients) and the control group (mitomycin C alone, 39 patients). In the treatment group, 5 KE Sapylin was injected intraperitoneally 48 h before operation and 4 mg of mitomycin C was injected into peritoneal cavity before the closure of the peritoneum. In the control group, only 4 mg mitomycin C was injected into peritoneal cavity before the closure of the peritonium.</p><p><b>RESULTS</b>There was no operative mortality or duodenal stump leakage in the two groups. Postoperative complications were anastomotic leakage (2.5%, 1/40) and incision rupture (2.5%, 1/40) in the treatment group, and incision rupture (2.6%, 1/39) in the control group, with no significant difference between the two groups (P > 0.05). The 3-year survival rate was significantly higher in the treatment group than in the control group (76.5% vs. 49.4%, P < 0.05).</p><p><b>CONCLUSIONS</b>Preoperative intraperitoneal injection of Sapylin can raise the 3-year survival rate after radical gastrectomy , without increasing the incidence rate of operative complications. Preoperative intraperitoneal injection of Sapylin is therefore a valuable therapy for advanced gastric cancer in clinic.</p>