Investigation Of The Changes Of Lymphangiogenesis Factor Expression And Biologic Behavior Of Gastric Cancer Cell By Blocking The EGFR/STAT3Signal Conduction Pathway

Objective:EGFR monoclonal antibody blocked EGFR activation and regulated the expression of STAT3, which could inhibit the expression of VEGF-C, and VEGF-D. To confirm that EGFR monoclonal antibody can inhibit lymph node metastasis on gastric cancer. To investigate the biological properties of various differentiated gastric cancer by blocking the EGFR/STAT3signal pathway. This research intends to play a guiding role in the diagnosis, treatment and prognosis of patients with various differentiated gastric carcinoma.Methods:1. In the research, MKN-28. SGC-7901、MGC-803and GES-1cells were fostered.2. The expression of EGFR in various differentiated gastric cancer was evaluated by flow cytometry and RT-PCR.3. The expression of EGFR mRNA in various differentiated gastric cancer cells was investigated with RT-PCR and immunohistochemistry before and after EGFR monoclonal antibody treatment.4. The cell apoptosis, cell proliferation, cell invasion, and cell cycle were evaluated in various differentiated gastric cancer cells which mediated by the EGFR monoclonal antibody treatment.5. Statistical data analysis was carried out using SPSS version17.0and differences were considered statistically significant whenp value was<0.05.Results:1. The study suggested that EGFR was over-expression in gastric cancer cells by flow cytometry and PT-PCR. The more poorly differentiated the cell was, the higher EGFR expression was demonstrated in gastric cancer cell.[MGC-803(poor differentiation)> SGC-7901(mediater differentiation)> MKN-28(higher differentiation)].2. EGFR expression was associated with the expression of STAT3、VEGF-C, and VEGF-D gastric cancere cells.3. The expression of STAT3、VEGF-C, and VEGF-D decreased significantly in the using anti-EGFR mono clone antibody group when compared with that in control group.4. EGFR monoclonal antibody could depress the proliferation, accelerate apoptosis, decrease cell invasion, and induce cell cycle arrest of the gastric cancer cells.Conclusions:1. The level of EGFR was high expression in gastric cancer cells. EGFR mRNA amplification was associated with the poor cell differentiation.2. EGFR monoclonal antibody could inhibit the protein and mRNA expression of STAT3, p-STAT3, VEGF-C, and VEGF-D in gastric cancer cells.3. EGFR monoclonal antibody played an important role in proliferation, apoptosis, invasiveness, and metastasis in gastric cancer cells.4. The biological properties changed markedly in poor differentiation of gastric cancer cells, by impeding the EGFR/STAT3signal transduction pathway.