Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/67618
Title: Proanthocyanidin-rich fractions from red rice extract enhance TNF-α-induced cell death and suppress invasion of human lung adenocarcinoma cell A549
Authors: Chayaporn Subkamkaew
Pornngarm Limtrakul
Supachai Yodkeeree
Keywords: Biochemistry, Genetics and Molecular Biology
Chemistry
Pharmacology, Toxicology and Pharmaceutics
Issue Date: 18-Sep-2019
Abstract: © 2019 by the authors. Tumor necrosis factor-alpha (TNF-α) plays a key role in promoting tumor progression, such as stimulation of cell proliferation and metastasis via activation of NF-κB and AP-1. The proanthocyanidin-rich fraction obtained from red rice (PRFR) has been reported for its anti-tumor effects in cancer cells. This study investigated the molecular mechanisms associated with PRFR on cell survival and metastasis of TNF-α-induced A549 human lung adenocarcinoma. Notably, PRFR enhanced TNF-α-induced A549 cell death when compared with PRFP alone and caused a G0-G1 cell cycle arrest. Although, PRFR alone enhanced cell apoptosis, the combination treatment induced the cells that had been enhanced with PRFR and TNF-α to apoptosis that was less than PRFR alone and displayed a partial effect on caspase-8 activation and PARP cleavage. By using the autophagy inhibitor; 3-MA attenuated the effect of how PRFR enhanced TNF-α-induced cell death. This indicates that PRFR not only enhanced TNF-α-induced A549 cell death by apoptotic pathway, but also by induction autophagy. Moreover, PRFR also inhibited TNF-α-induced A549 cell invasion. This effect was associated with PRFR suppressed the TNF-α-induced level of expression for survival, proliferation, and invasive proteins. This was due to reduce of MAPKs, Akt, NF-κB, and AP-1 activation. Taken together, our results suggest that TNF-α-induced A549 cell survival and invasion are attenuated by PRFR through the suppression of the MAPKs, Akt, AP-1, and NF-κB signaling pathways.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85072535172&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/67618
ISSN: 14203049
Appears in Collections:CMUL: Journal Articles

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