AI Article Synopsis
- Lung cancer, particularly non-small-cell lung cancer (NSCLC), is a prevalent and serious health issue; Urolithin A (UA) is a compound that may inhibit processes leading to cancer progression, but its exact mechanisms in NSCLC are not fully understood.
- This study explored UA's effects on NSCLC cells, specifically how it influences TMSB10, a significant protein related to cancer, by using various scientific methods to analyze cell behavior and protein interactions.
- The findings indicate that UA effectively reduces NSCLC cell growth and movement by promoting the breakdown of TMSB10 through autophagy, which disrupts normal cellular structures required for cell migration, suggesting UA's potential as a
Article Abstract
Background: Lung cancer is one of the most frequently diagnosed cancers and non-small-cell lung cancer (NSCLC) poses major diagnoses. Urolithin A (UA) is a natural compound produced by the gut microbiota through the metabolism of polyphenol ellagitannins (ETs) and ellagic acid (EA), which has been found to inhibit epithelial-mesenchymal transition (EMT) in lung cancer cell lines. However, the mechanism of UA function in NSCLC remains elusive.
Propose: This study aimed to investigate the potential effectiveness of UA in NSCLC therapeutic and uncovering its underlying mechanisms.
Methods: Effects of UA treatment, TMSB10 gene knockdown or overexpression on NSCLC cell phenotype were evaluated by availability, transwell assays. The downstream factors and pathways of UA were investigated by proteomics. TMSB10 expression in NSCLC tissues was detected by bioinformatics analysis as well as immunohistochemistry. Confocal imaging, GST pull-down and western blotting investigated the mechanism of UA induced TMSB10 degradation.
Results: In the present study, we demonstrated that UA shows an inhibitory role in NSCLC cell proliferation, migration, and invasion. This inhibition is attributed to the accelerated degradation of TMSB10, a biomarker among various cancers, via the autophagy-lysosome pathway. Additionally, knocked down of TMSB10 showed a similar phenotype with UA treatment. The reduction of TMSB10 protein level following decreased ATP level inhibits the F-actin formation for cell migration, thereby disrupting the equilibrium between G-actin-TMSB10 and G-actin-ATP interactions in A549 cells.
Conclusion: Our results reveal that UA is potential for NSCLC therapeutics through reducing the protein level of TMSB10 to deformation the F-actin.
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| http://dx.doi.org/10.1016/j.phymed.2024.156109 | DOI Listing |
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