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Relevant studies have indicated the association of HCG18 with tumour occurrence and progression. In this study, we observed that PM2.5 can enhance the growth of lung adenocarcinoma cells by modulating the expression of HCG18. Further investigations, including overexpression and knockout experiments, elucidated that HCG18 suppresses miR-195, which in turn upregulates the expression of ATG14, resulting in the upregulation of autophagy. Consequently, exposure to PM2.5 leads to elevated HCG18 expression in lung tissues, which in turn increases Atg14 expression and activates autophagy pathways through inhibition of miR-195, thereby contributing to oncogenesis.

Adenocarcinoma of Lung , Autophagy-Related Proteins , Autophagy , Disease Progression , Lung Neoplasms , MicroRNAs , Particulate Matter , MicroRNAs/genetics , MicroRNAs/metabolism , Humans , Adenocarcinoma of Lung/genetics , Adenocarcinoma of Lung/pathology , Adenocarcinoma of Lung/metabolism , Autophagy-Related Proteins/genetics , Autophagy-Related Proteins/metabolism , Lung Neoplasms/genetics , Lung Neoplasms/pathology , Lung Neoplasms/metabolism , Particulate Matter/adverse effects , Autophagy/genetics , Gene Expression Regulation, Neoplastic , Vesicular Transport Proteins/genetics , Vesicular Transport Proteins/metabolism , Cell Proliferation/genetics , A549 Cells , Cell Line, Tumor , Adaptor Proteins, Vesicular Transport

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