Pinostrobin, a fingerroot compound, regulates miR-181b-5p and induces acute leukemic cell apoptosis
Issued Date
2023-05-19
Resource Type
eISSN
20452322
Scopus ID
2-s2.0-85159670421
Pubmed ID
37208425
Journal Title
Scientific reports
Volume
13
Issue
1
Rights Holder(s)
SCOPUS
Bibliographic Citation
Scientific reports Vol.13 No.1 (2023) , 8084
Suggested Citation
Norkaew C., Subkorn P., Chatupheeraphat C., Roytrakul S., Tanyong D. Pinostrobin, a fingerroot compound, regulates miR-181b-5p and induces acute leukemic cell apoptosis. Scientific reports Vol.13 No.1 (2023) , 8084. doi:10.1038/s41598-023-35193-6 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/82874
Title
Pinostrobin, a fingerroot compound, regulates miR-181b-5p and induces acute leukemic cell apoptosis
Author's Affiliation
Other Contributor(s)
Abstract
Pinostrobin (PN) is the most abundant flavonoid found in fingerroot. Although the anti-leukemic properties of PN have been reported, its mechanisms are still unclear. MicroRNAs (miRNAs) are small RNA molecules that function in posttranscriptional silencing and are increasingly being used in cancer therapy. The aims of this study were to investigate the effects of PN on proliferation inhibition and induction of apoptosis, as well as the involvement of miRNAs in PN-mediated apoptosis in acute leukemia. The results showed that PN reduced cell viability and induced apoptosis in acute leukemia cells via both intrinsic and extrinsic pathways. A bioinformatics approach and Protein-Protein Interaction (PPI) network analysis revealed that ataxia-telangiectasia mutated kinase (ATM), one of the p53 activators that responds to DNA damage-induced apoptosis, is a crucial target of PN. Four prediction tools were used to predict ATM-regulated miRNAs; miR-181b-5p was the most likely candidate. The reduction in miR-181b-5 after PN treatment was found to trigger ATM, resulting in cellular apoptosis. Therefore, PN could be developed as a drug for acute leukemia; in addition, miR-181b-5p and ATM may be promising therapeutic targets.