Publication: Punicalagin, a pomegranate compound, induces apoptosis and autophagy in acute leukemia
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Issued Date
2021-11-02
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21678359
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2-s2.0-85118483701
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Mahidol University
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SCOPUS
Bibliographic Citation
PeerJ. Vol.9, (2021)
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Paweena Subkorn, Chosita Norkaew, Kamolchanok Deesrisak, Dalina Tanyong Punicalagin, a pomegranate compound, induces apoptosis and autophagy in acute leukemia. PeerJ. Vol.9, (2021). doi:10.7717/peerj.12303 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/75541
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Title
Punicalagin, a pomegranate compound, induces apoptosis and autophagy in acute leukemia
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Abstract
Background. Punicalagin is the major phenolic compound found in pomegranate peels. It has several reported medical benefits, including antioxidant, anti-inflammatory, and anticancer properties. The present study investigated the anti-leukemic effects and the molecular mechanism of punicalagin on NB4 and MOLT-4 leukemic cell lines. Methods. Leukemic cells were treated with punicalagin and cell viability was determined using MTS assay. Apoptosis and autophagy were analyzed by flow cytometry using Annexin V-FITC/PI and anti-LC3/FITC antibodies staining, respectively. Apoptotic and autophagic mRNA expression were determined using reverse transcription-quantitative PCR. STITCH bioinformatics tools were used to predict the interaction between punicalagin and its proposed target proteins. Results. Results indicated that punicalagin decreased NB4 and MOLT-4 cell viability in a dose-dependent manner. Punicalagin, in combination with daunorubicin, exhibited synergistic cytotoxic effects. Punicalagin induced apoptosis through the upregulation of caspase-3/-8/-9, Bax and the downregulation of Bcl-2 expression. Punicalagin also promoted autophagy via the downregulation of mTOR and the upregulation of ULK1 expression. Cyclooxygenase-2 and toll-like receptor 4 were found to be involved in punicalagin-induced cell death in punicalagin-targeted protein interactions. Conclusions. These results suggest that punicalagin exerts cytotoxic activities by suppressing proliferation and promoting apoptosis and autophagy by activating the caspase cascade, altering Bax and Bcl-2, and regulating autophagy via mTOR/ULK1 signaling.