This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractBackground: Our study aimed to investigate the association of polo-like kinase 4 (PLK4) expression with tumor features as well as survival in non-small cell lung cancer (NSCLC) patients.Methods: Five hundred and sixty NSCLC patients who underwent pulmonary resection were recruited, and their tumor specimens were obtained. Immunohistochemistry (IHC) staining was performed to assess PLK4 expression in tumor specimen. Follow-up documents were reviewed, and the disease-free survival (DFS) and overall survival (OS) were evaluated.Results: According to IHC staining, there were 277 (49.5%) patients with PLK4 low expression and 283 (50.5%) patients with PLK4 high expression. PLK4 high expression was further classified into three different classes: high+, high++, high+++, and 122 (21.8%), 127 (22.7%), 34 (6.1%) patients were with PLK4 high+, high++, high+++ expression, respectively. Polo-like kinase 4 expression was correlated with larger tumor size, LYN metastasis, and higher TNM stage. As for survival, DFS and OS were lower in patients with PLK4 high expression compared with patients with PLK4 low expression. In addition, DFS and OS were the lowest in patients with PLK4 high+++ expression, followed by those with PLK4 high++ expression, PLK4 high+ expression, and then patients with PLK4 low expression. Univariate and multivariate Cox's proportional hazard regression model analyses further disclosed that PLK4 was an independent predictive factor for poor DFS and OS in NSCLC patients. Conclusion:Our study preliminarily illuminates the clinical implication of PLK4 in NSCLC, while further studies are still needed to explicit the value of PLK4 in surveillance and treatment of NSCLC. K E Y W O R D Sdisease-free survival, non-small cell lung cancer, overall survival, polo-like kinase 4, tumor features

The bioactivity of microRNA‐1827 (miR‐1827) in lung adenocarcinoma cells would be explored. The expression level of gene and miR‐1827 in 76 pairs of lung adenocarcinoma tissues and adjacent counterparts were analyzed by a quantitative real‐time polymerase chain reaction. Primary lung adenocarcinoma cells were derived from patients’ tissues. These cells were treated with miR‐1827 agomir to mimic the upregulation of endogenous miR‐1827. The malignant degree of lung adenocarcinoma cells in vitro was evaluated by cell proliferation, colony formation, transwell invasion, and apoptosis assays. Western blot analysis was used to observe the transition of lung adenocarcinoma cells from epithelial‐to‐mesenchymal. Target genes of miR‐1827 were predicted by bioinformatics analysis. In addition, the interaction between miR‐1827 and candidate messenger RNAs was verified by dual‐luciferase reporter assay and AGO2‐RNA immunoprecipitation. Besides, the effect of miR‐1827 on tumors was verified by in vivo experiments. Transient gene overexpression was achieved by plasmids transfection. In this study, we found that the expression of miR‐1827 was downregulated in lung adenocarcinoma, and its low expression was significantly correlated with the progression of lung adenocarcinoma and poor prognosis of patients. miR‐1827 overexpression remarkably reduced the malignancy of primary lung adenocarcinoma cells in vitro. MYC and FAM83F were identified as two targeted genes of miR‐1827 in lung adenocarcinoma cells. The levels of these two genes were upregulated in lung adenocarcinoma, and their high expression was significantly associated with the progression of lung adenocarcinoma and poor prognosis of patients. Overexpression of MYC or FAM83F attenuated the effects of miR‐1827 on primary lung adenocarcinoma cells in vitro. In addition, in vivo experiments showed that miR‐1827 inhibited tumor growth by reducing the levels of MYC and FAM83F. In conclusion, miR‐1827 might repress the development of lung adenocarcinoma by targeting oncogenic genes MYC and FAM83F.

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