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Background: Lung cancer is one of the most common causes of cancer death among all the malignancies worldwide. Evidences suggest that the incidence and mortality of lung cancer has been on the rise. MicroRNA-449a (miR-449a) as one important member of microRNAs, has been demonstrated acting as a tumor suppressor in lung cancer. In this study, we sought to assess the relationship between miR-449a expression level and diagnostic value of lung cancer.Methods: In this present research, quantitative Real-Time PCR was applied to detect the miR-449a expression in 116 lung cancer patients and 41 healthy volunteers. The diagnostic value of miR-449a in lung cancer patients was determined by receiver operating characteristic (ROC) curve.Results: MiR-449a was significantly down-regulated in lung cancer patients compared with healthy control (PmiR-449a expression was associated with sex (P=0.004), tumor size (P=0.000), TNM stage (P=0.006) and metastasis (P=0.036). However, there was no correlation with age, smoking history and histological type of lung cancer patients (all P＞0.05). In the ROC analysis, the results showed that the area under the ROC curve (AUC) was 0.902 with the sensitivity of 94.8% and specificity of 78.0%, and the optimum cutoff value was 2.255.Conclusion: MiR-449a expression was down-regulated in lung cancer patients, and it could be an efficient diagnostic biomarker in lung cancer patients.

To study the mRNA expression level of growth inhibition factor 4 (ING4) and hypoxia inducing factor 1 alpha (HIF-1 alpha), and their relationship with tumor malignant degree or the pathology classification in human brain astrocytoma.The mRNA expression levels of ING4 and HIF-1 alpha were detected by RT-PCR method in 45 cases of grade I-IV human brain astrocytoma and 11 cases of control brain tissues from January 2009 to June 2010 in the Second Affiliated Hospital of Zhengzhou University, and their correlation was also analyzed.In the non-tumor brain tissue, the expression level of ING4 mRNA was 1.19 ± 0.22, while they were 0.91 ± 0.19, 0.74 ± 0.28, 0.54 ± 0.33 and 0.22 ± 0.19 in I-IV grade astrocytoma, respectively. Compared with the non-tumor control, the mRNA expression level of ING4 gene decreased significantly in the astrocytoma (P0.05). And the expression of ING4 gradually reduced with the increase of the pathological classification of the astrocytoma.In the non-tumor brain tissue, the expression level of HIF-1 alpha mRNA was 0.26 ± 0.16, and they were 0.34 ± 0.19, 0.50 ± 0.23, 0.96 ± 0.15 and 1.04 ± 0.15 in I-IV grade astrocytoma, respectively.For HIF-1 alpha gene, the mRNA expression level increased significantly in the astrocytoma. Meanwhile, the expression gradually increased with the increase of the pathological classification of the astrocytoma (P0.05). The mRNA expression showed a negative correlation between ING4 and HIF-1 alpha with the increase of the tumor malignant degree.The ING4 and HIF-1 alpha genes play a role in the tumorigenesis and development of human brain astrocytoma, and closely associate with the malignant degree of astrocytoma.

Objective: To investigate the effect of isoliquiritigenin on the activity of DNA topoisomerase (TOP I) and its inhibitory effect on the growth of U87 glioma cells. Methods: This study investigated the inhibitory effect of isoliquiritigenin on the growth of U87 glioma cells and its cytotoxicity by MTT method and determined the effect of isoliquiritigenin on TOP I activity by agarose gel electrophoresis. On this basis, we studied the interaction between isoliquiritigenin and TOP I and DNA. Finally, we further discussed the effect of isoliquiritigenin on the activity of Caspase 3, the apoptosis protein of U87 glioma cells. Results: Isoliquiritigenin could inhibit the growth of U87 glioma cells (half inhibitory concentration IC50: 0.221 mM) and is of low cytotoxicity to normal cells. Agarose gel electrophoresis showed that isoliquiritigenin had significant inhibitory effect on TOP I activity. Molecular simulation results indicated that isoliquiritigenin took priority of binding to the active center of TOP I, and formed hydrogen bonds with the catalytic site Try723. Finally, Caspase 3 activity detection results suggested that isoliquiritigenin could significantly increase the activity of Caspase 3 (P < 0.05). Conclusion: Isoliquiritigenin had a reversible inhibitory effect on TOP I activity, reduced the rate of single strand DNA unwinding in tumor cells, and thus played an important role in inducing the apoptosis of U87 glioma cells.