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p14ARF, a tumor suppressor protein, encoded by the p16 tumor suppressor gene, has been reported to be associated with the clinicopathological features of lung cancer. However, the evaluated outcomes were inconsistent and remained inconclusive. In this study, we conducted a meta-analysis to clarify the significance of p14ARF expression in lung cancer pathogenesis. Materials and methods: Electronic databases, PubMed, Web of Knowledge, Embase, and CNKI, were retrieved to collect relevant articles with inclusion and exclusion criteria. Using Stata 12.0 software, 95% confidence intervals (CIs) and odds ratios (ORs) were calculated. Results: A total of 15 eligible case-control studies that evaluated the relationship between p14ARF expression and lung cancer were included in the meta-analysis. The results demonstrated that there were significant associations between p14ARF expression and the risk of non-smallcell lung cancer (NSCLC), lung adenocarcinoma, and lung squamous carcinoma (for NSCLC, OR =11.02, 95% CI =5.30-22.92; for lung adenocarcinoma, OR =7.28, 95% CI =3.92-13.50; and for lung squamous carcinoma, OR =14.40, 95% CI =2.83-73.24). In the stratified analysis based on race, significant associations between p14ARF expression and lung cancer risk were found in Chinese population and Caucasians (for Chinese population, OR = 7.02, 95% CI =4.48-11.00 and for Caucasians, OR =4.19, 95% CI =1.42-12.38). Furthermore, the expression of p14ARF was significantly associated with the TNM-stage of lung cancer in Chinese population (OR =2.07, 95% CI =1.38-3.10). Conclusion: p14ARF expression was significantly associated with the risk of lung cancer. In addition, the data of the meta-analysis showed that there was a significant correlation between p14ARF expression and the TNM-stage of lung cancer in Chinese population. [ABSTRACT FROM AUTHOR]

Background: In this study, we investigated the functional correlation between microRNA-210 (miR-210) and gene of F-box protein 31 (FBXO31) in regulating breast cancer. Methods: Dual-luciferase assay and quantitative real-time polymerase chain reaction were used to investigate the binding of miR-210 with FBXO31 and their expression patterns in breast cancer. miR-210 was inhibited in breast cancer T47D and MCF-7 cells to assess its effect on cancer proliferation, cell cycle progression, and migration. FBXO31 was also downregulated in breast cancer cells to examine its effect on miR-210-mediated breast cancer regulation. The interaction between miR-210 and FBXO31 was further investigated by examining the effect of overexpressing miR-210 on FBXO31-induced suppression of breast cancer proliferation. Results: FBXO31 was the downstream target gene of miR-210 in breast cancer. miR-210 and FBXO31 are inversely expressed in breast cancer cell lines. miR-210 downregulation reduced cancer progression, induced cell cycle arrest, and inhibited cancer migration in T47D and MCF-7 cells. Tumor suppression by miR-210 downregulation was reversed by downregulating FBXO31. In FBXO31-overexpressed breast cancer cells, upregulating miR-210 also reversed the tumorsuppressive effect of FBXO31 on breast cancer proliferation. Conclusion: Our work demonstrated that the expression pattern and tumor regulatory functions of miR-210 and FBXO31 are inversely correlated in breast cancer. [ABSTRACT FROM AUTHOR]