Background The present study aimed to evaluate the difference in microbiota diversity in the oral cavity and fluid bronchoalveolar lavage (BALF) of patients with lung cancer. Material/Methods Buccal (saliva) and lower respiratory tract BALF samples were collected from 51 patients with primary bronchogenic carcinoma and 15 healthy controls, and bacterial genomic DNA was extracted. High-throughput 16S rDNA amplicon sequencing was performed, and microbial diversity, composition, and functions of microbiota were analyzed by bioinformatics methods. Results Patients with lung cancer have lower microbial diversity than healthy controls in both saliva and BALF samples. Significant segregation was observed between the different pathological types of lung cancer groups and the control group regardless of the sampling site. Treponema and Filifactor were identified as potential bacterial biomarkers in BALF samples, while Filifactor was ideal to distinguish healthy controls from lung cancer patients. Moreover, the predictive variation analysis of the KEGG (Kyoto Encyclopedia of Genes and Genomes) metabolic pathway showed that the metabolic differences in microbiota varied by sampling site. Conclusions Lung cancer patients carry a different and less diverse microorganism community than healthy controls. Certain bacterial taxa might be associated with lung cancer, but the exact species depends on the sampling site and the pathological type. This study provides basic data on the microbiota diversity in BALF and saliva samples from lung cancer patients. Further investigation with a larger sample size should help validate the enriched species in different pathological types of lung cancers.

These authors contributed equally to this workBackground: The fat mass and obesity-associated protein (FTO) was identified as a critical demethylase involved in regulating cellular mRNA stability by removing N6methyladenosine (m6A) residues from mRNA. Emerging evidence has revealed that FTO is deeply implicated in lung cancer. However, knowledge of the function of FTO in lung adenocarcinoma (LUAC) is limited. Methods: FTO and FTO R96Q (R96Q), an FTO missense mutant lacking demethylase activity, were ectopically overexpressed, and FTO was knocked down via siRNA in A549 and H1299 cells. The relationships between FTO with cell characteristics and mRNA m6A levels were explored. Furthermore, RNA sequencing was performed on A549 cells. Results: FTO overexpression enhanced the proliferation, migration, and invasion ability of A549 and H1299 cells, decreased mRNA m6A levels. Interestingly, overexpression of R96Q, blunted the effects of FTO overexpression on cell proliferation and invasion. Through RNA sequencing analysis of A549 cells overexpressing FTO or R96Q and control A594 cells, 45 genes were identified as affected by m6A mRNA demethylation. Most of these genes were related to lung cancer, such as laminin γ2, thrombospondin 1, nerve growth factor inducible, integrin alpha11, and proprotein convertase subtilisin/kexin type 9. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses suggested that these genes are fundamental to cancer development processes, such as cell migration and extracellular matrix organization. Conclusion: Our research shows that FTO facilitates LUAC cell progression by activating cell migration through m6A demethylation; however, further research on the mechanism underlying FTO activity in LUAC is necessary.

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