Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/80287
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dc.contributor.authorSong, Len_US
dc.contributor.authorHuang, YMen_US
dc.contributor.authorHou, XDen_US
dc.contributor.authorYang, YHen_US
dc.contributor.authorKala, Sen_US
dc.contributor.authorQiu, ZHen_US
dc.contributor.authorZhang, Ren_US
dc.contributor.authorSun, Len_US
dc.date.accessioned2019-01-30T09:14:40Z-
dc.date.available2019-01-30T09:14:40Z-
dc.date.issued2018-
dc.identifier.citationCellular physiology and biochemistry, 2018, v. 49, no. 5, p. 1825-1839en_US
dc.identifier.issn1015-8987-
dc.identifier.urihttp://hdl.handle.net/10397/80287-
dc.description.abstractBackground/Aims: Sonodynamic therapy (SDT), based on the synergistic effect of low-intensity ultrasound and sonosensitizer, is a potential approach for non-invasive treatment of cancers. In SDT, mitochondria played a crucial role in cell fate determination. However, mitochondrial activities and their response to SDT remain elusive. The purpose of this study was to examine the response of mitochondria to SDT in tumor cells.en_US
dc.description.abstractMethods: A human breast adenocarcinoma cell line - MCF-7 cells were subjected to 5-aminolevulinic acid (ALA)-SDT, with an average ultrasonic intensity of 0.25W/cm(2). Mitochondrial dynamics and redox balance were examined by confocal immunofluorescence microscopy and western blot. The occurrence of mitophagy was determined by confocal immunofluorescence microscopy.en_US
dc.description.abstractResults: Our results showed that ALA-SDT could induce mitochondrial dysfunction through mitochondrial depolarization and fragmentation and lead to mitophagy. The Parkin-dependent signaling pathway was involved and promoted resistance to ALA-SDT induced cell death. Finally, excessive production of ROS was found to be necessary for the initiation of mitophagy.en_US
dc.description.abstractConclusion: Taken together, we conclude that ROS produced by 5-ALA-SDT could initiate PINK1/Parkin-mediated mitophagy which may exert a protective effect against 5-ALA-SDTinduced cell death in MCF-7 cells.en_US
dc.description.sponsorshipDepartment of Biomedical Engineeringen_US
dc.language.isoenen_US
dc.publisherKargeren_US
dc.relation.ispartofCellular physiology and biochemistryen_US
dc.rights2018 The Author(s)en_US
dc.rightsThis article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND) (http://www.karger.com/Services/OpenAccessLicense). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission.en_US
dc.rightsThe following publication Song, L., Huang, Y.M., Hou, X.D., Yang, Y.H., Kala, S., Qiu, Z.H., ... & Sun, L. (2018). PINK1/Parkin-mediated mitophagy promotes resistance to sonodynamic therapy. Cellular physiology and biochemistry, 49 (5), 1825-1839 is available at https://dx.doi.org/10.1159/000493629en_US
dc.subjectSonodynamic therapyen_US
dc.subjectMitophagyen_US
dc.subjectROSen_US
dc.subjectMitochondrial dynamicsen_US
dc.subjectPINK1/Parkin signaling pathwayen_US
dc.titlePINK1/Parkin-mediated mitophagy promotes resistance to sonodynamic therapyen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage1825-
dc.identifier.epage1839-
dc.identifier.volume49-
dc.identifier.issue5-
dc.identifier.doi10.1159/000493629-
dc.identifier.isiWOS:000447182000013-
dc.identifier.scopus2-s2.0-85053939566-
dc.identifier.pmid30231241-
dc.identifier.eissn1421-9778-
dc.description.validate201901 bcrc-
dc.description.oapublished_final-
Appears in Collections:Journal/Magazine Article
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