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Article: Induction of S phase cell arrest and caspase activation by polysaccharide peptide isolated from Coriolus versicolor enhanced the cell cycle dependent activity and apoptotic cell death of doxorubicin and etoposide, but not cytarabine in HL-60 cells.

TitleInduction of S phase cell arrest and caspase activation by polysaccharide peptide isolated from Coriolus versicolor enhanced the cell cycle dependent activity and apoptotic cell death of doxorubicin and etoposide, but not cytarabine in HL-60 cells.
Authors
Issue Date2005
PublisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htm
Citation
Oncology Reports, 2005, v. 14 n. 1, p. 145-155 How to Cite?
AbstractActivation of the cell death program (apoptosis) is a strategy for the treatment of human cancer, and unfortunately a large number of drugs identified as cell cycle-specific agents for killing cancer cells are also toxic to normal cells. The present study demonstrates that the polysaccharide peptide (PSP) extracted from the Chinese medicinal mushroom, Coriolus versicolor, used in combination therapy in China, has the ability to lower the cytotoxicity of certain anti-leukemic drugs via their interaction with cell cycle-dependent and apoptotic pathways. Flow cytometry analysis demonstrated that pre-treatment of PSP (25-100 microg/ml) dose-dependently enhanced the cell cycle perturbation and apoptotic activity of doxorubicin (Doxo) and etoposide (VP-16), but not cytarabine (Ara-C) in human promyelocytic leukemia HL-60 cells. The antagonistic result from combined treatment with Ara-C and PSP may be caused by the removal of HL-60 cells in the G1-S boundary by PSP before exposure to Ara-C. A negative correlation between the increase in apoptotic cell population (pre-G1 peak) with the S-phase cell population expression (R2=0.998), the expression of cyclin E expression (R2=0.872) and caspase 3 activity (R2=0.997) suggests that PSP enhanced the apoptotic machinery of Doxo and VP-16 in a cell cycle-dependent manner and is mediated, at least in part, by the PSP-mediated modulation of the regulatory checkpoint cyclin E and caspase 3. This study is the first to describe the cell cycle mechanistic action of PSP and its interaction with other anticancer agents. Our data support the potential development of PSP as an adjuvant for leukemia treatment, but also imply the importance of understanding its interaction with individual anticancer agents.
Persistent Identifierhttp://hdl.handle.net/10722/84931
ISSN
2015 Impact Factor: 2.486
2015 SCImago Journal Rankings: 0.968
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHui, KPen_HK
dc.contributor.authorSit, WHen_HK
dc.contributor.authorWan, JMen_HK
dc.date.accessioned2010-09-06T08:58:47Z-
dc.date.available2010-09-06T08:58:47Z-
dc.date.issued2005en_HK
dc.identifier.citationOncology Reports, 2005, v. 14 n. 1, p. 145-155en_HK
dc.identifier.issn1021-335Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/84931-
dc.description.abstractActivation of the cell death program (apoptosis) is a strategy for the treatment of human cancer, and unfortunately a large number of drugs identified as cell cycle-specific agents for killing cancer cells are also toxic to normal cells. The present study demonstrates that the polysaccharide peptide (PSP) extracted from the Chinese medicinal mushroom, Coriolus versicolor, used in combination therapy in China, has the ability to lower the cytotoxicity of certain anti-leukemic drugs via their interaction with cell cycle-dependent and apoptotic pathways. Flow cytometry analysis demonstrated that pre-treatment of PSP (25-100 microg/ml) dose-dependently enhanced the cell cycle perturbation and apoptotic activity of doxorubicin (Doxo) and etoposide (VP-16), but not cytarabine (Ara-C) in human promyelocytic leukemia HL-60 cells. The antagonistic result from combined treatment with Ara-C and PSP may be caused by the removal of HL-60 cells in the G1-S boundary by PSP before exposure to Ara-C. A negative correlation between the increase in apoptotic cell population (pre-G1 peak) with the S-phase cell population expression (R2=0.998), the expression of cyclin E expression (R2=0.872) and caspase 3 activity (R2=0.997) suggests that PSP enhanced the apoptotic machinery of Doxo and VP-16 in a cell cycle-dependent manner and is mediated, at least in part, by the PSP-mediated modulation of the regulatory checkpoint cyclin E and caspase 3. This study is the first to describe the cell cycle mechanistic action of PSP and its interaction with other anticancer agents. Our data support the potential development of PSP as an adjuvant for leukemia treatment, but also imply the importance of understanding its interaction with individual anticancer agents.en_HK
dc.languageengen_HK
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htmen_HK
dc.relation.ispartofOncology reportsen_HK
dc.titleInduction of S phase cell arrest and caspase activation by polysaccharide peptide isolated from Coriolus versicolor enhanced the cell cycle dependent activity and apoptotic cell death of doxorubicin and etoposide, but not cytarabine in HL-60 cells.en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1021-335X&volume=14&spage=145&epage=155&date=2005&atitle=Induction+of+S+phase+cell+arrest+and+caspase+activation+by+polysaccharide+peptide+isolated+from+Coriolus+versicolor+enhanced+the+cell+cycle+dependent+activity+and+apoptotic+cell+death+of+doxorubicin+and+etoposide,+but+not+cytarabine+in+HL-60+cellsen_HK
dc.identifier.emailWan, JM: jmfwan@hku.hken_HK
dc.identifier.authorityWan, JM=rp00798en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid15944782-
dc.identifier.scopuseid_2-s2.0-24644507326en_HK
dc.identifier.hkuros100003en_HK
dc.identifier.volume14en_HK
dc.identifier.issue1en_HK
dc.identifier.spage145en_HK
dc.identifier.epage155en_HK
dc.identifier.isiWOS:000229920500023-
dc.publisher.placeGreeceen_HK
dc.identifier.scopusauthoridHui, KP=24492032000en_HK
dc.identifier.scopusauthoridSit, WH=8528923000en_HK
dc.identifier.scopusauthoridWan, JM=8930305000en_HK

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