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Article: Sonoporation induces apoptosis and cell cycle arrest in human promyelocytic leukemia cells

TitleSonoporation induces apoptosis and cell cycle arrest in human promyelocytic leukemia cells
Authors
KeywordsApoptosis
Cell cycle arrest
Cell signaling
Sonoporation
Issue Date2011
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/ultrasmedbio
Citation
Ultrasound In Medicine And Biology, 2011, v. 37 n. 12, p. 2149-2159 How to Cite?
AbstractDespite being a transient biophysical phenomenon, sonoporation is known to disturb the homeostasis of living cells. This work presents new evidence on how sonoporation may lead to antiproliferation effects including cell-cycle arrest and apoptosis through disrupting various cell signaling pathways. Our findings were obtained from sonoporation experiments conducted on HL-60 human promyelocytic leukemia cells (with 1% v/v microbubbles; 1 MHz ultrasound; 0.3 or 0.5MPa peak negative pressure; 10% duty cycle; 1 kHz pulse repetition frequency; 1 min exposure period). Membrane resealing in these sonoporated cells was first verified using scanning electron microscopy. Time-lapse flow cytometry analysis of cellular deoxyribonucleic acid (DNA) contents was then performed at four post-sonoporation time points (4 h, 8 h, 12 h and 24 h). Results indicate that an increasing trend in the apoptotic cell population can be observed for at least 12 h after sonoporation, whilst viable sonoporated cells are found to temporarily accumulate in the G 2/M (gap-2/mitosis) phase of the cell cycle. Further analysis using western blotting reveals that sonoporation-induced apoptosis involves cleavage of poly adenosine diphosphate ribose polymerase (PARP) proteins: a pro-apoptotic hallmark related to loss of DNA repair functionality. Also, mitochondrial signaling seems to have taken part in triggering this cellular event as the expression of two complementary regulators for mitochondrial release of pro-apoptotic molecules, Bcl-2 (B-cell lymphoma 2) and Bax (Bcl-2-associated X), are seen to be imbalanced in sonoporated cells. Furthermore, sonoporation is found to induce cell-cycle arrest through perturbing the expression of various cyclin and Cdk (cyclin-dependent kinase) checkpoint proteins that play an enabling role in cell-cycle progression. These bioeffects should be taken into account when using sonoporation for therapeutic purposes. © 2011 World Federation for Ultrasound in Medicine & Biology.
Persistent Identifierhttp://hdl.handle.net/10722/155706
ISSN
2015 Impact Factor: 2.298
2015 SCImago Journal Rankings: 0.885
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhong, Wen_HK
dc.contributor.authorSit, WHen_HK
dc.contributor.authorWan, JMFen_HK
dc.contributor.authorYu, ACHen_HK
dc.date.accessioned2012-08-08T08:34:55Z-
dc.date.available2012-08-08T08:34:55Z-
dc.date.issued2011en_HK
dc.identifier.citationUltrasound In Medicine And Biology, 2011, v. 37 n. 12, p. 2149-2159en_HK
dc.identifier.issn0301-5629en_HK
dc.identifier.urihttp://hdl.handle.net/10722/155706-
dc.description.abstractDespite being a transient biophysical phenomenon, sonoporation is known to disturb the homeostasis of living cells. This work presents new evidence on how sonoporation may lead to antiproliferation effects including cell-cycle arrest and apoptosis through disrupting various cell signaling pathways. Our findings were obtained from sonoporation experiments conducted on HL-60 human promyelocytic leukemia cells (with 1% v/v microbubbles; 1 MHz ultrasound; 0.3 or 0.5MPa peak negative pressure; 10% duty cycle; 1 kHz pulse repetition frequency; 1 min exposure period). Membrane resealing in these sonoporated cells was first verified using scanning electron microscopy. Time-lapse flow cytometry analysis of cellular deoxyribonucleic acid (DNA) contents was then performed at four post-sonoporation time points (4 h, 8 h, 12 h and 24 h). Results indicate that an increasing trend in the apoptotic cell population can be observed for at least 12 h after sonoporation, whilst viable sonoporated cells are found to temporarily accumulate in the G 2/M (gap-2/mitosis) phase of the cell cycle. Further analysis using western blotting reveals that sonoporation-induced apoptosis involves cleavage of poly adenosine diphosphate ribose polymerase (PARP) proteins: a pro-apoptotic hallmark related to loss of DNA repair functionality. Also, mitochondrial signaling seems to have taken part in triggering this cellular event as the expression of two complementary regulators for mitochondrial release of pro-apoptotic molecules, Bcl-2 (B-cell lymphoma 2) and Bax (Bcl-2-associated X), are seen to be imbalanced in sonoporated cells. Furthermore, sonoporation is found to induce cell-cycle arrest through perturbing the expression of various cyclin and Cdk (cyclin-dependent kinase) checkpoint proteins that play an enabling role in cell-cycle progression. These bioeffects should be taken into account when using sonoporation for therapeutic purposes. © 2011 World Federation for Ultrasound in Medicine & Biology.en_HK
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/ultrasmedbioen_HK
dc.relation.ispartofUltrasound in Medicine and Biologyen_HK
dc.subjectApoptosisen_HK
dc.subjectCell cycle arresten_HK
dc.subjectCell signalingen_HK
dc.subjectSonoporationen_HK
dc.subject.meshApoptosis - Radiation Effectsen_US
dc.subject.meshCell Cycle Checkpoints - Radiation Effectsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshElectroporation - Methodsen_US
dc.subject.meshHigh-Energy Shock Wavesen_US
dc.subject.meshHumansen_US
dc.subject.meshLeukemia, Promyelocytic, Acute - Pathology - Physiopathologyen_US
dc.subject.meshRadiation Dosageen_US
dc.subject.meshSonicationen_US
dc.titleSonoporation induces apoptosis and cell cycle arrest in human promyelocytic leukemia cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailWan, JMF: jmfwan@hku.hken_HK
dc.identifier.emailYu, ACH: alfred.yu@hku.hken_HK
dc.identifier.authorityWan, JMF=rp00798en_HK
dc.identifier.authorityYu, ACH=rp00657en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.ultrasmedbio.2011.09.012en_HK
dc.identifier.pmid22033133-
dc.identifier.scopuseid_2-s2.0-82955162759en_HK
dc.identifier.hkuros193624-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-82955162759&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume37en_HK
dc.identifier.issue12en_HK
dc.identifier.spage2149en_HK
dc.identifier.epage2159en_HK
dc.identifier.eissn1879-291X-
dc.identifier.isiWOS:000297324700021-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhong, W=46761637400en_HK
dc.identifier.scopusauthoridSit, WH=8528923000en_HK
dc.identifier.scopusauthoridWan, JMF=8930305000en_HK
dc.identifier.scopusauthoridYu, ACH=8699317700en_HK
dc.identifier.citeulike9972101-

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