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PM 2.5 regulates the progression of lung adenocarcinoma through the axis of HCG18, miR-195 and ATG14.
- Source :
-
Clinical and experimental pharmacology & physiology [Clin Exp Pharmacol Physiol] 2024 Jun; Vol. 51 (6), pp. e13861. - Publication Year :
- 2024
-
Abstract
- Relevant studies have indicated the association of HCG18 with tumour occurrence and progression. In this study, we observed that PM <subscript>2.5</subscript> 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 PM <subscript>2.5</subscript> 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.<br /> (© 2024 John Wiley & Sons Australia, Ltd.)
- Subjects :
- Humans
A549 Cells
Adaptor Proteins, Vesicular Transport drug effects
Adaptor Proteins, Vesicular Transport metabolism
Cell Line, Tumor
Cell Proliferation genetics
Gene Expression Regulation, Neoplastic
Vesicular Transport Proteins genetics
Vesicular Transport Proteins metabolism
HLA Antigens drug effects
HLA Antigens metabolism
Adenocarcinoma of Lung genetics
Adenocarcinoma of Lung pathology
Adenocarcinoma of Lung metabolism
Autophagy genetics
Autophagy-Related Proteins drug effects
Autophagy-Related Proteins genetics
Autophagy-Related Proteins metabolism
Disease Progression
Lung Neoplasms genetics
Lung Neoplasms pathology
Lung Neoplasms metabolism
MicroRNAs genetics
MicroRNAs metabolism
Particulate Matter adverse effects
Subjects
Details
- Language :
- English
- ISSN :
- 1440-1681
- Volume :
- 51
- Issue :
- 6
- Database :
- MEDLINE
- Journal :
- Clinical and experimental pharmacology & physiology
- Publication Type :
- Academic Journal
- Accession number :
- 38724488
- Full Text :
- https://doi.org/10.1111/1440-1681.13861