RESUMO
@#Objective To evaluate the effect of smoking and drinking status on the prognosis of patients with esophageal squamous cell carcinoma (ESCC). Methods The clinical data of 483 patients with ESCC who underwent surgical treatment in Shannxi Provincial People's Hospital from 2007 to 2016 were retrospectively analyzed. Among them, 352 patients were male and 131 were female, with a median age of 64 (37-80) years. There were 311 smokers and 172 drinkers. The relationship between preoperative drinking or smoking status and the clinicopathological characteristics of patients with ESCC was analyzed. Log-rank method and Cox risk regression were used to conduct univariate and multivariate survival analysis, respectively. Results The preoperative smoking status was related to the patient's tumor location (P=0.030). Drinking status was associated with tumor location (P=0.001), degree of differentiation (P=0.030), pathological T stage (P=0.024) and pathological N stage (P=0.029). Univariate survival analysis showed that smoking status did not affect the disease-free survival (DFS) (P=0.188) and overall survival (OS) (P=0.127) of patients with ESCC. However, patients who drank alcohol had worse PFS than non-drinking patients (29.37 months vs. 42.87 months, P=0.009). It was further proved that alcohol consumption was an independent risk factor affecting patients' recurrence and metastasis by using multivariate analysis (RR=1.28, P=0.040). Alcohol consumption also reduced the OS of patients by 21.47 months (P=0.014), however, multivariate analysis did not yield significant results. Conclusion Preoperative drinking status is related to the stage and differentiation of patients with ESCC. It is an independent risk factor affecting the recurrence and metastasis of ESCC.
RESUMO
Objective To investigate the effects of CNTN-1 on the invasion and migration of human esophageal cancer EC9706 cells and the possible mechanism.Methods The expression of CNTN-1 in human esophageal cancer EC9706 cells was measured by qPCR and Western blot.After transfection with CNTN-1 siRNA or CNTN-1, the cells were divided into control group, scrambled siRNA group, CNTN-1 siRNA group, pcDNA3.1-vector group and pcDNA3.1-CNTN-1 group.Cell proliferation, invasion and migration were respectively analyzed by BrdU assay and Transwell test.The expression of MMP-2 and MMP-9 were detected by qPCR and Western blot.Results The mRNA and protein expression of CNTN-1 were significantly upregulated in EC9706 cells.Compared with control, cell proliferation, invasion and migration, as well as the expression of MMP-2 and MMP-9 were significantly decreased by CNTN-1 siRNA, while they were increased by CNTN-1 overexpression (P<0.05).ConclusionsCNTN-1 can influence the invasion and metastasis of esophageal cancer cells through the regulation of the expression of MMP-2 and MMP-9.
RESUMO
Background and purpose: Previous studies have confirmed that the expression of leucine-rich repeat-containing 3B (CLRRC3B) was significantly decreased in different human cancers, which was also associated with the migration and invasion of cancer cells. The aim of this study was to explore the potential mechanism of LRRC3B in the development of esophageal cancer. Methods: The LRRC3B expression was detected in 60 cancer tissues and 60 adjacent non-neoplastic tissues by immunohistochemistry. The mRNA and protein expression of LRRC3B in Eca109 and HEECs were detected using real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) and Western blot, respectively. Eca109 cells with different treatments were divided into three groups:normal group, negative control group (transfected with pCMV6 plasmid), overexpression LRRC3B group (transfected with pCMV6-LRRC3B plasmid). Transwell assay was used to measure the migration and invasion of Eca109 cells in different groups. The protein levels of E-cadherin, N-cadherin, Vimentin and p-Akt were determined by Western blot. Results: The expression of LRRC3B in esophageal cancer tissues was lower than that of non-cancerous tissues, as well as the expression of LRRC3B in Eca109 was decreased compared with that of normal esophageal epithelial cell line HEEC. Overexpression of LRRC3B significantly inhibited Eca109 cells migration and invasion, upregulated the expression of E-cadherin and decreased the expression of N-cadherin and Vimentin. Moreover, overexpression of LRRC3B significantly inhibited the phosphorylation of Akt in Eca109 cells. Conclusion: The expression of LRRC3B was decreased in esophageal cancer. Overexpression of LRRC3B can efficiently inhibit the EMT progression in esophageal cancer cells by suppressing PI3K/Akt signaling pathway.