PD-L1 rs2890658 Polymorphism Increases Risk for Non-Small-Cell Lung Cancer in Northern China Population Based on Experimental Data and Meta-Analysis.

Purpose: To dig the PD-L1 rs2890658 polymorphism with susceptibility of non-small-cell lung cancer (NSCLC) in northern China. Patients and Methods. There were 600 NSCLC patients and 600 age and sex matched controls from the same ethnic origin recruited in the present research. Polymerase chain reaction-restriction fragment length polymorphism method genotyped PD-L1 rs2890658 polymorphism. PubMed and Embase were searched to get eligible literature for meta-analysis. The association between PD-L1 rs2890658 polymorphism and NSCLC risk was calculated with odds ratio and 95% confidence interval. Results: It is more likely that individuals who have CC genotype and C allele are 2.15 and 1.41 times to develop NSCLC compared with individuals with AA genotype and A allele, respectively. Meta-analysis showed that the individuals who have C allele and CA genotype increased the risk of suffering from NSCLC. Conclusion: PD-L1 rs2890658 polymorphism increased NSCLC risk in northern China population and it might predict the occurrence of NSCLC.

Ligustrazine eases lung cancer by regulating PTEN and Wnt/ß-catenin pathway.

BACKGROUND: Lung cancer (LC) is the most common malignant tumor in the world. Ligustrazine (LSZ), an alkaloid, is an active ingredient extracted from chuanxiong Hort. Earlier studies suggested that LSZ plays a crucial role in lung diseases. The study aimed to investigate the detailed mechanism of LSZ on LC. METHODS: Protein expression was determined by qPCR, western blotting and immunohistochemistry. Cell viability was determined by CCK8 assay. Invasiveness was detected by Transwell assay. Cell growth was determined by clone formation assay. Male BALB/c nude mice were randomly divided into 2 groups (n=10): LSZ group and Control group. RESULTS: Results showed that PTEN is low-expressed in lung tumor tissues and LC cells (H1650, A549, H1299, and PC-9). Appropriate doses of LSZ could significantly promote the expression of PTEN in LC cells. Besides, LSZ inhibits invasion and proliferation of H1299 cells. However, knockdown PTEN counteracts the inhibitory effect. Animal experiments suggest that LSZ inhibits tumor formation in vivo. Mechanistically, western blotting shows that LSZ treatment significantly decreased the levels of Wnt and ß-catenin, while increasing the levels of PTEN and GSK-3ß. CONCLUSIONS: Collectively, these results demonstrate that LSZ ameliorates LC by down-regulating PTEN level and blocking Wnt/ß-catenin signaling pathway.