Journal
ANTICANCER RESEARCH
Volume 40, Issue 6, Pages 3209-3220Publisher
INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.14302
Keywords
Lung cancer; tannic acid; intrinsic apoptosis; G(0)/G(1) cell cycle arrest
Categories
Funding
- National Research Foundation of Korea (NRF) - Korean government (MSIT) [2018R1C1B6006146]
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [2018R1D1A1B07048651, 2019R1I1A1A01060399, 2019R1I1A1A01060537]
- National Research Foundation of Korea [2018R1D1A1B07048651, 2019R1I1A1A01060399, 2019R1I1A1A01060537, 2018R1C1B6006146] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Background/Aim: Non-small cell lung cancer (NSCLC) is one among the most common cancers worldwide. Recently, dietary phytochemicals have been reported as an attractive approach to improve the symptoms of NSCLC patients. Tannic acid is a natural polyphenol, which is known to have anticancer effects on in vitro models of breast, gingival and colon cancer. However, the molecular mechanisms associated with the actions of tannic acid on A549 human lung cancer cells have not been elucidated. Materials and Methods: In this study, we analyzed the effect of tannic acid on A549 cells and their underlying mechanisms using western blotting, flow cytometry, invasion assay and tumorsphere formation assay. Results: Tannic acid treatment suppressed the viability of A549 cells through cell cycle arrest and induction of the intrinsic pathways of apoptosis. In addition, the various malignant phenotypes of A549 cells including invasion, migration, and stemness were inhibited by tannic acid treatment. Conclusion: Tannic acid could be used as an effective inhibitor of lung cancer progression.
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