In the recent two decades, three global viral infectious diseases, severe acute respiratory syndrome (SARS), middle east respiratory syndrome (MERS), and coronavirus disease (COVID-19), have occurred worldwide. SARS occurred in November 2002, causing 8096 infected cases, as well as 774 deaths. MERS occurred in June, 2012, causing 2519 confirmed cases, along with 866 associated deaths. COVID-19 occurred in December 2019, as of 30 April 2020, a total of 3,024,059 clinical cases have been reported, including 208,112 deaths. Healthcare workers (HCWs) need to be in close contact with these virus-infected patients and their contaminated environments at work, thus leading to be infected in some of them, even a few of them are died in line of duty. In this review, we summarized the infection status of HCWs during the outbreak of SARS, MERS and COVID-19, with in-depth discussion, hoping to provoke sufficient attention to the HCWs infection status by more people.

Benzo(a)pyrene (BaP), an important toxic component of cigarette smoke, can cause lung cancer and lead to the progression of lung cancer. In the present study, we investigated the effect of BaP on the migration of lung adenocarcinoma A549 cells. BaP (1 µM) promoted the migration of A549 cells in a time-dependent manner and upregulated the expression of the Twist family BHLH transcription factor 1 (Twist1). BaP also induced upregulation of the mesenchymal markers N-cadherin and vimentin and downregulation of the epithelial marker E-cadherin. When the expression of Twist1 was knocked down in A549 cells that were treated with BaP for 4 weeks (A549BaP-4w), the expression of Twist1 decreased, which inhibited the migration capacity of A549BaP-4w cells, the expression of N-cadherin and vimentin was downregulated and the expression of E-cadherin was upregulated. In addition, morphological observations of A549BaP-4w cells revealed that the epithelial characteristics of A549 cells became mesenchymal characteristics. When the expression of Twist1 was knocked down, the A549BaP-4w cells were transformed back to cells with epithelial characteristics. In conclusion, the results from the present study indicate that BaP enhances the epithelial-mesenchymal transition-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1.

Background: To comprehensively understand the impact of sex and smoking on the efficacy of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) therapy in terms of overall survival (OS) in non-small-cell lung cancer (NSCLC). Methods: PubMed, Cochrane Library, Embase, and Scopus were searched from inception to March 17, 2019. OS was analyzed based on hazard ratios (HRs) and 95% confidence intervals (CIs) and estimated using the random effects model. Results: Our meta-analysis included 22 studies involving 11,874 patients. In the primary analysis, we found no statistically significant efficacy difference for EGFR-TKI intervention between females and males (pooled HR 0.95, 95% CI 0.87–1.04, P = 0.30) and no obvious efficacy difference between never smokers and ever smokers (pooled HR 0.91, 95% CI 0.76–1.09, P = 0.31). In the subgroup analysis of placebo control treatment, we found that female NSCLC patients who received EGFR-TKI therapy had a longer OS than male patients (pooled HR 0.86, 95% CI 0.75–1.00, P = 0.04), while smoking status showed no significant effect on the efficacy of EGFR-TKI treatment in terms of the OS of NSCLC patients in all subgroup analyses. Conclusion: The efficacy of EGFR-TKI therapy for NSCLC patients is independent of smoking status but dependent on sex, and females have a longer OS than males.

Background Lung cancer is a common malignant tumour and the leading cause of cancer death. Smoking is closely related to lung cancer, which can not only induce the occurrence of lung cancer but also affect its progress and prognosis. Objectives To investigated the relationship between smoking and 14-3-3σ protein expression in non-small-cell lung cancer (NSCLC), investigated the relationship between 14-3-3σ expression and cell migration in A549 cells induced by cigarette smoke extract (CSE) and explored whether DNA methylation plays a role in the decreased expression of 14-3-3σ induced by CSE. Methods 14-3-3σ protein expression was examined by immunohistochemistry in 152 NSCLC tissue samples. In vitro experiments were divided into three groups: The current smoking group (CS), the ex-smoking group (ES) and the normal control group (NC). Cell transfection was used for 14-3-3σ protein overexpression. The mRNA and protein expression levels of 14-3-3σ were detected by RT-PCR and Western blotting, respectively. Cell migration was detected by Transwell and wound-healing assays, and the methylation of 14-3-3σ was detected by methylation-specific PCR. Results 14-3-3σ protein expression was decreased in NSCLC patients with a history of smoking. The expression of 14-3-3σ was decreased in A549 cells treated with CSE. The migration capacity of A549 cells treated with CSE was enhanced. DNA methylation in the cigarette smoke-treated A549 cells was higher than that in the untreated cells. Conclusion Cigarette smoke induced reduction of 14-3-3σ expression can promote the progression of non-small cell lung cancer.