RESUMO
OBJECTIVE: To investigate the independent factors affecting the prognosis of patients after resection of esophageal cancer, and to inquire into the relationship between GSTM1, GSTT1 gene polymorphisms and esophageal cancer prognosis. METHODS: The clinical data of 273 patients with esophageal cancer were retrospectively analyzed. The patients were followed-up after their surgery, and the gene polymorphisms of GSTM1 and GSTT1 in each individual were detected by polymerase chain reaction (PCR). The clinical features along with the gene polymorphisms of GSTM1 and GSTT1 associated with the prognosis of patients were analyzed by using the method of univariate analysis and Cox proportional hazard model. The cumulative survival rate was estimated by Kaplan-Meier methods, and the survival curves were compared by using the log-rank test. RESULTS: The overall cumulative survival rate of first year, third year and fifth year is 94.6%, 58.5% and 17.8%, respectively. The median survival time (MST) is 38.7 months. The results of univariate analysis showed that: infiltration depth, length of tumor, the number of lymph node metastasis, the region of lymph node metastasis and the genetic polymorphism of GSTM1 and GSTT1 gene loci were associated with the survival of postoperative patients. Cox multivariate analysis further indicated that the length of tumor, the number of lymph node metastasis and the combined genotype (1) [GSTM1 (+/+) or (+/-) & GSTT1 (-/-)] were the independent prognostic factors. The length of tumor, the number of lymph node metastasis were the risk factors for the prognosis, and the combined genotype (1) had protective effect on survival when compared with reference [GSTM1 (+/+) or (+/-) & GSTT1 (+/+) or (+/-)]. CONCLUSION: The length of tumor, the number of lymph node metastasis were confirmed as the independent prognostic factors of esophageal carcinoma, and the null genotypes for GSTT1 (-/-) might be a protective factor for survival and GSTM1 (-/-) might be a potential negative prognostic factor in patients with esophageal cancer.
RESUMO
OBJECTIVE: To investigate the effects of α-Enolase (ENO1) over-expression on the proliferative and migratory abilities of AGS cells. METHODS: The target gene was cloned and mounted to the eukaryotic expression vector pcDNA3.1(+), then was transfected into gastric cancer cell lines AGS. mRNA and protein level of ENO1 in AGS cells were verified by real-time quantitative RT-PCR and Western Blot, respectively. The effects of over-expression of ENO1 on proliferative and migratory abilities of AGS cells were detected by the experiments of CCK-8, colony formation and wound healing assays. RESULTS: The eukaryotic expression vector pcDNA3.1(+)/eno1 was successfully constructed, and verified by sequencing. It was shown from the cell proliferation curves that the proliferative ability of AGS-ENO1 transfected group was higher than that of the control group after 72 hours (t = 3.44, P = 0.04), meanwhile, the number of the cell-colonies of the AGS-ENO1 group were significantly greater than that of the control group (t = 5.26, P = 0.01). For the ability of migration, it was significantly enhanced in the over-expression ENO1 cells than in the negative cells (t = 7.35, P < 0.001). CONCLUSION: The over-expression of ENO1 protein can enhance the abilities of proliferation and migration in gastric cancer cells of AGS, which indicates that ENO1 may be an important potential tumor-marker associated with the development of gastric cancer.
