The present study indicated downregulation of E-cadherin was significantly correlated with poor OS and DFS/PFS, additionally, downregulation of E-cadherin was associated with invasive phenotype in NSCLC. Based on the above points, we thought our up-to date meta-analysis was worthwhile and comprehensive. Various subgroup analyses were done. When we limited to the race, HR estimate, sample size, percentage of reduced/negative Ecadherin, and histological type, all these subgroups suggested the significant association between E-cadherin expression and poor OS. In addition, when we focus to stage I NSCLC, downregulated E-cadherin expression was associated with survival, suggesting this prognostic factor could also be of importance in early-stage NSCLC. What��s more, E-cadherin expression was also related to poor DFS/PFS. In additional, downregulated E-cadherin expression was correlated with poor grade of differentiation, positive lymph node metastasis, positive vascular invasion, and advanced TNM stages, ASP1517 indicating downregulated E-cadherin in NSCLC presented invasive phenotypes. As a result, poor survival is very likely the consequence. All these evidence we observed demonstrated that E-cadherin was closely related to progression of NSCLC. Our analysis provided the evidence that E-cadherin maybe a prognostic factor in NSCLC patients. However, as neoplastic progression is a complex and multiple-step process, E-cadherin may only play a small role. Combining E-cadherin with other biomarkers would be more meaningful and efficient, Also, genegene and gene-environment interaction showed be taken into consideration. Beside, E-cadherin may serve as a novel target and the application of individualized management in NSCLC patients. As loss of E-cadherin expression may associate with neoplastic progression, reconstitution of E-cadherin expression maybe an apparent attractive approach for treatment of NSCLC. This would be possible to prevent E-cadherin promoter methylation in some cases. In addition, the signalling LY2157299 pathways such as such as HER receptors and Notch downstream targets are aberrantly activated in consequence of E-cadherin loss.