The present study aimed to explore the effects of stromal interaction molecule 1 (STIM1) knockdown on the migration, invasion and metastasis of A549 cells in vitro and in vivo. Western blotting and immunohistochemistry were used to detect protein expression levels. Wound healing and Transwell invasion assays were used to assess the migratory and invasive abilities of A549 cells transfected with STIM1‑specific short hairpin (sh)RNA (shSTIM1). In addition, a tail vein metastatic assay was performed. The results demonstrated that the frequency of STIM1 high‑expression was significantly increased in metastatic lung cancer tissues (72.2%) compared with in non‑metastatic lung cancer tissues (33.0%). STIM1 knockdown inhibited A549 cell migration and invasion in vitro and tumor metastasis in vivo. The protein expression levels of Snail1, Vimentin, matrix metalloproteinase (MMP) 2 and MMP9 were markedly decreased in A549‑shSTIM1 compared with in A549 cells transfected with control shRNA (shcon). In addition, the protein expression levels of E‑cadherin were markedly increased in A549‑shSTIM1 cells compared with in A549‑shcon cells. These results suggested that STIM1 knockdown may inhibit the migration and invasion of A549 cells in vitro, and metastasis in vivo.

Previous studies have reported the association of glutathione S-transferase M1 (GSTM1) deletion polymorphism with genetic susceptibility of lung cancer in Chinese population. However, the results remained controversial. The aim of this study was to clarify the association of GSTM1 deletion polymorphism with lung cancer risk in Chinese population. Systematic searches were performed through the search engines of Medline/Pubmed, Web of Science, EMBASE, CNKI and Wanfang Medical Online. The pooled effects were calculated by STATA 10.0 software package and Review Manager 5.0.24. Overall, we observed an association of GSTM1 deletion polymorphism with increased lung cancer risk in Chinese population (odds ratio (OR) = 1.46, 95% confidence interval (95%CI): 1.32–1.66 for null genotype vs. present genotype) based on 53 studies including 7,833 cases and 10,353 controls. We also observed an increased risk of GSTM1 null genotype for lung cancer in stratified analyses by source of control, smoking status and histological type. The findings suggest that GSTM1 deletion polymorphism may contribute to lung cancer risk in Chinese population. Further, well-designed studies with larger sample sizes are required to verify the results.