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Background: Aspirin is a classic anti‐inflammatory drug and its anticancer effect has been previously explored in many types of cancer including colorectal cancer therapy. Programmed cell death‐ligand 1 (PD‐L1) is widely expressed in tumor cells and displays an inhibitory role in antitumor immunity. This study aimed to clarify the role of PD‐L1 in aspirin‐suppressed lung cancer. Methods: The inhibitory effect of aspirin on lung cancer cell proliferation was assessed using an MTT cell viability assay. The role of aspirin in the modulation of PD‐L1 expression was analyzed by western blot or RT‐PCR assays. In lung cancer cells, the influence of aspirin on PD‐L1 promoter activity was detected using a luciferase reporter assay. The interaction of TAZ with PD‐L1 promoter in the cells, with or without aspirin administration, was tested via chromatin immunoprecipitation (ChIP) analysis. The function of PD‐L1 in aspirin‐mediated growth inhibition of lung cancer was examined using a cell viability assay. Results: Following treatment with aspirin, lung cancer cell growth was markedly suppressed. Aspirin was able to markedly decrease the expression of PD‐L1 at the mRNA and protein levels in lung cancer cells. For the mechanism study, we found that the promoter of PD‐L1 was inactivated by aspirin via TAZ transcriptional coactivator in the cells. With regard to the functional investigation, aspirin was capable of resisting cell proliferation and PD‐L1 overexpression abolished aspirin‐depressed cell proliferation in lung cancer. Conclusions: Aspirin suppressed the growth of lung cancer cells via targeting the TAZ/PD‐L1 axis. [ABSTRACT FROM AUTHOR]

Introduction: It is clinically challenging to infer the phylogenetic relationship between different tumor lesions of patients with multiple synchronous lung cancers (MSLC), whether these lesions are the result of independently evolved tumor or intrapulmonary metastases. Methods: We used the Illumina X10 platform to sequence 128 stage I lung cancer samples collected from 64 patients with MSLC. All samples were analyzed for mutation spectra and phylogenetic inference. Results: We detected genetic aberrations within genes previously reported to be recurrently altered in lung adenocarcinoma including, EGFR, ERBB2, TP53, BRAF, and KRAS. Other putative driver mutations identified were enriched in RTK‐RAS signaling, TP53 signaling, and cell cycle. Also, we found some interesting cases, two cases that carried EGFR L858R and T790M co‐mutation in one tumor and another tumor with only EGFR 19del, and 1 case with two KRAS hotspots in the same tumor. Due to the short follow‐up time and early stage, further investigation is needed to determine whether this unique mutation profile will affect their progression‐free survival (PFS) and overall survival (OS). Regarding genetic evolution analysis among 64 tumor samples, 50 of them display distinct mutational profiles, suggesting these are independently evolved tumors, which is consistent with histopathological assessment. On the other hand, six patients were identified to be intrapulmonary metastasis as the mutations harbored in different lesions are clonally related. Conclusion: In summary, unlike intrapulmonary metastases, patients with MSLC harbor distinct genomic profiles in different tumor lesions, and we could distinguish MSLC from intrapulmonary metastases via clonality estimation. [ABSTRACT FROM AUTHOR]

Coal not only powers the household, social and global economy development but also emits large pollutants. Natural gas and electricity can be promising solutions to the energy supply and environmental pollution dilemma in Hebei Province of China. Currently, this coal‐dependent province has launched the Hebei Air Pollution Prevention and Control Program to curb air pollution by replacing residential coal consumption with natural gas and electricity for space heating in winter. Approximately 2.53 million households have completed the switch from coal‐burning stoves to natural gas or electricity stoves in rural areas surrounding Beijing and Tianjin since 2017. However, the contribution of this clean heating replacement on provincial emission reduction remains unclear. This study aimed to determine emission factors, energy efficiency, and economic profits of traditional coal‐burning stoves, as well as cleaner natural gas and electricity stoves by laboratory simulation and field tests. The results indicated a significant reduction after clean replacement for PM2.5, CO, CO2, NOX,SO2, CH4, and 16 types of U.S. EPA priority polycyclic aromatic hydrocarbons (PAHs). The emission of PM2.5 can be reduced by 99% and 95% for natural gas and electricity switch. Toxic equivalent quantity value of PAHs was also decreased from 4.89 (coal) to 0.03 (natural gas) and 0.07 μg/MJnet (electricity). When comprehensively considering the upstream pollutants emissions from power plant, natural gas switching performed better than coal‐fired electricity. Moreover, the government supported the clean heating replacement project with extensive financial subsidy for purchasing clean stoves and using clean energy within 3 years in rural areas. A relatively cheaper price on an energy basic of natural gas and electricity use can be obtained after this subsidy compared to coal. Air pollution of Hebei Province and the policy of replacing residential coal with natural gas or electricity for space heating from the national to local government level were reviewed. The emission characteristics and economic performance of coal burning and clean stoves were evaluated and the air quality of clean heating replacement and nonreplacement regions were compared. [ABSTRACT FROM AUTHOR]