Journal
CELLS
Volume 9, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/cells9020282
Keywords
Tannic acid; Wnt/beta-catenin; mitochondrial ROS; TRAIL; extrinsic apoptosis pathway
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 [2019R1I1A1A01060399, 2019R1I1A1A01060537]
- National Research Foundation of Korea [2019R1I1A1A01060537, 2018R1C1B6006146, 2019R1I1A1A01060399] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Human embryonic carcinoma (EC; NCCIT) cells have self-renewal ability and pluripotency. Cancer stem cell markers are highly expressed in NCCIT cells, imparting them with the pluripotent nature to differentiate into other cancer types, including breast cancer. As one of the main cancer stem cell pathways, Wnt/beta-catenin is also overexpressed in NCCIT cells. Thus, inhibition of these pathways defines the ability of a drug to target cancer stem cells. Tannic acid (TA) is a natural polyphenol present in foods, fruits, and vegetables that has anti-cancer activity. Through Western blotting and PCR, we demonstrate that TA inhibits cancer stem cell markers and the Wnt/beta-catenin signaling pathway in NCCIT cells and through a fluorescence-activated cell sorting analysis we demonstrated that TA induces sub-G1 cell cycle arrest and apoptosis. The mechanism underlying this is the induction of mitochondrial reactive oxygen species (ROS) (mROS), which then induce the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated extrinsic apoptosis pathway instead of intrinsic mitochondrial apoptosis pathway. Moreover, ribonucleic acid sequencing data with TA in NCCIT cells show an elevation in TRAIL-induced extrinsic apoptosis, which we confirm by Western blotting and real-time PCR. The induction of human TRAIL also proves that TA can induce extrinsic apoptosis in NCCIT cells by regulating mROS.
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