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Yang Chen, Wei Wang, Lizhong Zeng, Ke Mi, Na Li, Jie Shi, Shuanying Yang Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, People’s Republic of ChinaCorrespondence: Shuanying YangDepartment of Respiratory Medicine, The Second Affiliated Hospital, Xi’an Jiaotong University School of Medicine in Xi’an, Shaanxi, People’s Republic of ChinaTel +86-13991392919Email yangshuanying666@163.comBackground: Neutrophil-lymphocyte ratio (NLR) is a novel marker of inflammation. Emerging studies have evaluated the relationship of NLR with cardiovascular diseases and malignant conditions. However, rare studies regarded the association between NLR and long-term health status. This study aimed to evaluate the association of NLR with all-cause mortality and cause-specific mortality among adults in the United States.Methods: We obtained eight cycles data of National Health and Nutrition Examination Surveys (NHANES) from 1999 to 2014, and enrolled 32328 participants after certain screening. By weighted chi-square test and linear regression analysis, we analyzed the correlation between NLR and baseline characteristics of the participants. Kaplan–Meier curves and Cox regression models were used to assess the survival relevance of NLR. We conducted stratified analysis, interaction analysis, and sensitivity analysis to robustness of our results.Results: Participants with high NLR levels had a higher risk of death. After adjustment for baseline characteristics, the hazard ratio comparing the higher vs lower NLR levels was 1.43 (95% CI, 1.18– 1.73) for all-cause mortality, 1.27 (95% CI, 0.84– 1.92) for cancer mortality, and 1.44 (95% CI, 0.96– 2.16) for cardiovascular disease mortality. Stratified analysis found that the observed associations between NLR levels and mortality did not differ significantly.Conclusion: In this nationally representative cohort of US adults, higher NLR was significantly associated with an increased risk of all-cause mortality.Keywords: inflammation, lymphocyte, neutrophil, mortality

MiR-22-3p has been reported to be down-regulated in several cancers, but its expression pattern and roles in lung cancer is unclear. Given the crucial role of microRNAs in cancer progression, we examined the expression and function of miR-22-3p in lung adenocarcinoma. MiR-22-3p expression in lung cancer tissues and cell lines was measured by qRT-PCR. Cell proliferation was measured by WST-1 and colony formation assays were used to reveal the role of miR-22-3p in lung cancer in vitro. MiR-22-3p was notably down-regulated in lung cancer tissues as compared to normal lung tissues, but it was not associated with the clinical characteristics of tumor stage, differentiation and patient’s smoking status. Colony formation ability and cell proliferation were suppressed by miR-22-3p mimics in lung cancer cell lines. Mechanistically, miR-22-3p mimics could reduce MET and STAT3 protein expression and induce apoptosis as measured by PARP protein. We conclude that miR-22-3p may play a tumor suppressor role via inhibiting MET-STAT3 signaling and have potential to be a therapeutic target and biomarker in lung adenocarcinoma.

Background and ObjectiveInterstitial lung disease with lung cancer (ILD-LC) is rare and its management has not been fully described. This study aimed to investigate the management and prognosis of ILD-LC patients in China.MethodsThe present analysis is a retrospective real-world cohort study. Clinical data of ILD-LC patients were obtained from 3 hospitals in China. The overall survival (OS) of patients was analyzed. Univariate and multivariate regression analyses were performed.ResultsOne hundred eighty-four ILD-LC patients included were biased toward male (85.3%), smokers (75.5%), idiopathic pulmonary fibrosis (IPF) (58.2%) patients with comorbidities (67.9%) and ECOG-PS score of 1 (65.2%). Most patients were advanced peripheral non-small cell lung cancer. The initial anti-cancer regimen for ILD-LC is mainly chemotherapy, and patients with early-stage LC prefer surgery. In the anti-cancer cohort, the number of ILD-LC patients who underwent the 2nd and 3rd or more anti-cancer regimens were 78 (55.7%) and 32 (22.8%), respectively. In the non-anticancer cohort, the median OS was 3.5 months. In the early-stage cohort, the median OS was 14.2 months in the systematic therapy group; however, the median OS was not reached in the surgery group. In the advanced-stage cohort with systematic therapy, the median OS was 7.2 months. Interstitial pneumonia (IIP) and anti-angiogenesis were associated with OS in the univariate analysis, whereas anti-angiogenesis was an independent protective factor for advanced LC with ILD.ConclusionPatients with ILD-LC have very poor prognosis. Appropriate anti-tumor treatment can prolong the survival time of patients who can tolerate it. Targeted therapy and immunotherapy are alternative treatments for LC patients with mild ILD. For ILD patients with advanced LC, antiangiogenic regimens significantly improve the prognosis of the disease.

Additional file 2: Figure S1. A luciferase reporter assay was used to detect the luciferase activity of LUC-cPVT1 in T293 cells transfected with miRNA mimics to identify miRNAs that bind to the circPVT1 sequence. Data are shown as mean ± SD, ***P

Additional file 5: Figure S4. Assessment of proliferation in H520 cells transfected with NC, si-CCNF-1, siCCNF-2, si-CCNF-3 by CCK-8 assay. *P

Additional file 1: Table S1. Sequences of primers used in this study. Table S2. Sequences of siRNAs used in this study.

Additional file 4: Figure S3. qRT-PCR analysis of mRNA expression in H520 cells after treatment with si-cPVT1–1 and si-cPVT1–2.