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Non-small cell lung cancer (NSCLC) is a major type of human lung cancer and the primary cause of cancer-associated cases of mortality worldwide. Phosphatase and tensin homolog (PTEN) is a potent tumor suppressor gene in various human cancer types. The aim of the current study was to explore the role of PTEN and its associated regulatory mechanisms in NSCLC. Firstly, the expression of PTEN was detected using western blotting in a variety of NSCLC cell lines. The results revealed that compared with normal control cells, PTEN levels were significantly decreased in NSCLC cell lines (P<0.01). Short hairpin (sh)RNAs specific to PTEN were also used to knockdown endogenous PTEN in NSCLC cells. The results indicated that cell viability was significantly increased in PTEN-knockdown cells compared with those transfected with negative control shRNA (P<0.01). Conversely, overexpression of PTEN in A549 and SK-MES-1 cells significantly decreased the optical density of NSCLC cells (P<0.01). Flow cytometry was used to investigate the cell cycle; the results revealed that PTEN knockdown significantly increased the percentage of cells at G 0 /G 1 phase (P<0.01) and decreased the number of cells at S phase (P<0.01). The molecular mechanism was further explored using western blotting and the results demonstrated that PTEN overexpression increased the levels of cleaved caspase-3 (P<0.01). These results suggest that PTEN may be a potential target gene for gene therapy in patients with NSCLCs.

Aims: The renin-angiotensin-aldosterone system is important to the development of atrial fibrillation (AF). A lot of research has focused on the relationship between angiotensin-converting enzyme (ACE) insertion (I) /deletion (D) gene polymorphisms and AF, with inconsistent results. A meta-analysis was carried out to find the correlation between ACE I/D gene polymorphisms and AF. Methods: Data were extracted from articles published before September 2013 on ACE I/D polymorphisms and AF in Embase, PubMed, WanFangData, and China National Knowledge Infrastructure. Results: The recessive model found that ACE I/D gene polymorphisms were related to AF (odds ratio (OR) = 1.61, 95% confidence interval (CI) = 1.16–1.72). Subgroup analysis showed a significant association in the recessive model for Asian (OR = 1.40, 95% CI = 1.19–1.80) and Caucasian (OR = 1.42, 95% CI = 1.01–1.99) populations. Conclusions: ACE I/D gene polymorphisms and AF are significantly related to ethnicity. Individuals with the ACE D/D genotype appear to be at higher risk of AF.