Liposome‑delivered baicalein induction of myeloid leukemia K562 cell death via reactive oxygen species generation

Article

Wang, S., Wen, S., Bell, C. and Appiah, S. 2018. Liposome‑delivered baicalein induction of myeloid leukemia K562 cell death via reactive oxygen species generation. Molecular Medicine Reports. 17 (3), pp. 4524-4530. https://doi.org/10.3892/mmr.2018.8396
TypeArticle
TitleLiposome‑delivered baicalein induction of myeloid leukemia K562 cell death via reactive oxygen species generation
AuthorsWang, S., Wen, S., Bell, C. and Appiah, S.
Abstract

Baicalein (BL), a potential cancer chemopreventative flavone, has been reported to inhibit cancer cell growth by inducing apoptosis and causing cell cycle arrest in various human cancer cell models. Delivery of BL via nanoliposomes has been shown to improve its oral bioavailability and long‑circulating property in vivo. However, the role of BL in the inhibition of human chronic myeloid leukemia (CML) K562 cell growth and its underlying mechanisms has yet to be elucidated. In the present study, BL was formulated into liposomes with different sizes to improve its solubility and stability. The cytotoxic and pro‑apoptotic effects of free BL and liposomal BL were also evaluated. The results demonstrated that 100 nm liposomes were the most stable formulation when compared with 200 and 400 nm liposomes. Liposomal BL inhibited K562 cell growth as efficiently as free BL (prepared in DMSO), indicating that the liposome may be a potential vehicle to deliver BL for the treatment of CML. Flow cytometry analysis showed that there was significant (P<0.005) cell cycle arrest in the sub‑G1 phase (compared with vehicle control), indicating cell apoptosis following 20 µM liposomal BL or free BL treatment of K562 cells for 48 h. The induction of cell apoptosis by all BL preparations was further confirmed through the staining of treated cells with Annexin V‑fluorescein isothiocyanate/propidium iodide. A significant increase in reactive oxygen species (ROS) gene­ration was observed in free BL and liposomal BL treated cells, with a higher level of ROS produced from those treated with free BL. This indicated that cell apoptosis induced by BL may be via ROS generation and liposome delivery may further extend the effect through its long‑circulating property.

KeywordsMolecular Medicine; Genetics; Biochemistry; Cancer Research; Oncology; Molecular Biology; baicalein; liposomes; chronic myeloid leukemia; cell cycle; apoptosis; reactive oxygen species
PublisherSpandidos Publications
JournalMolecular Medicine Reports
ISSN1791-2997
Electronic1791-3004
Publication dates
Online08 Jan 2018
Print31 Mar 2018
Publication process dates
Deposited19 Jan 2018
Accepted18 Dec 2017
Output statusPublished
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Copyright Statement

Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) License.

Digital Object Identifier (DOI)https://doi.org/10.3892/mmr.2018.8396
Web of Science identifierWOS:000424400000138
LanguageEnglish
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