File Download
  • No File Attached
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer
  • Basic View
  • Metadata View
  • XML View
TitlePhloroglucinol derivative MCPP induces cell apoptosis in human colon cancer
 
AuthorsHuang, SM2 3
Cheung, CW1
Chang, CS2
Tang, CH2
Liu, JF2
Lin, YH2
Chen, JH4
Ko, SH
Wong, KL3 2 1
Lu, DY
 
Issue Date2011
 
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503
 
CitationJournal of Cellular Biochemistry, 2011, v. 112 n. 2, p. 643-652 [How to Cite?]
DOI: http://dx.doi.org/10.1002/jcb.22966
 
AbstractThis study is the first to investigate the anticancer effects of the new phloroglucinol derivative (3,6-bis(3-chlorophenylacetyl)phloroglucinol; MCPP) in human colon cancer cells. MCPP induced cell death and antiproliferation in three human colon cancer, HCT-116, SW480, and Caco-2 cells, but not in primary human dermal fibroblast cells. MCPP-induced concentration-dependent apoptotic cell death in colon cancer cells was measured by fluorescence-activated cell sorter (FACS) analysis. Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2alpha (eIF-2alpha), suggesting the induction of ER stress. MCPP also increased GSK3alpha/beta(Tyr270/216) phosphorylation and reduced GSK3alpha/beta(Ser21/9) phosphorylation time-dependently. Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP-mediated cell apoptosis. Treatment of MCPP also increased caspase-7, caspase-9, and caspase-3 activity. The inhibition of caspase activity by z-DEVE-FMK or z-VAD-FMK significantly reduced MCPP-induced apoptosis. Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation. Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3alpha/beta activation in mediating the MCPP-induced human colon cancer cell apoptosis. © 2010 Wiley-Liss, Inc.
 
ISSN0730-2312
2012 Impact Factor: 3.062
2012 SCImago Journal Rankings: 1.261
 
DOIhttp://dx.doi.org/10.1002/jcb.22966
 
ISI Accession Number IDWOS:000287071900033
Funding AgencyGrant Number
National Science Council98-2320-B-039-009-MY2
98-2627-B-039-005
China Medical University HospitalDMR-99-152
Funding Information:

Grant sponsor: National Science Council; Grant numbers: 98-2320-B-039-009-MY2, 98-2627-B-039-005; Grant sponsor: China Medical University Hospital; Grant number: DMR-99-152.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorHuang, SM
 
dc.contributor.authorCheung, CW
 
dc.contributor.authorChang, CS
 
dc.contributor.authorTang, CH
 
dc.contributor.authorLiu, JF
 
dc.contributor.authorLin, YH
 
dc.contributor.authorChen, JH
 
dc.contributor.authorKo, SH
 
dc.contributor.authorWong, KL
 
dc.contributor.authorLu, DY
 
dc.date.accessioned2011-09-23T05:42:19Z
 
dc.date.available2011-09-23T05:42:19Z
 
dc.date.issued2011
 
dc.description.abstractThis study is the first to investigate the anticancer effects of the new phloroglucinol derivative (3,6-bis(3-chlorophenylacetyl)phloroglucinol; MCPP) in human colon cancer cells. MCPP induced cell death and antiproliferation in three human colon cancer, HCT-116, SW480, and Caco-2 cells, but not in primary human dermal fibroblast cells. MCPP-induced concentration-dependent apoptotic cell death in colon cancer cells was measured by fluorescence-activated cell sorter (FACS) analysis. Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2alpha (eIF-2alpha), suggesting the induction of ER stress. MCPP also increased GSK3alpha/beta(Tyr270/216) phosphorylation and reduced GSK3alpha/beta(Ser21/9) phosphorylation time-dependently. Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP-mediated cell apoptosis. Treatment of MCPP also increased caspase-7, caspase-9, and caspase-3 activity. The inhibition of caspase activity by z-DEVE-FMK or z-VAD-FMK significantly reduced MCPP-induced apoptosis. Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation. Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3alpha/beta activation in mediating the MCPP-induced human colon cancer cell apoptosis. © 2010 Wiley-Liss, Inc.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationJournal of Cellular Biochemistry, 2011, v. 112 n. 2, p. 643-652 [How to Cite?]
DOI: http://dx.doi.org/10.1002/jcb.22966
 
dc.identifier.doihttp://dx.doi.org/10.1002/jcb.22966
 
dc.identifier.epage652
 
dc.identifier.hkuros193530
 
dc.identifier.isiWOS:000287071900033
Funding AgencyGrant Number
National Science Council98-2320-B-039-009-MY2
98-2627-B-039-005
China Medical University HospitalDMR-99-152
Funding Information:

Grant sponsor: National Science Council; Grant numbers: 98-2320-B-039-009-MY2, 98-2627-B-039-005; Grant sponsor: China Medical University Hospital; Grant number: DMR-99-152.

 
dc.identifier.issn0730-2312
2012 Impact Factor: 3.062
2012 SCImago Journal Rankings: 1.261
 
dc.identifier.issue2
 
dc.identifier.pmid21268086
 
dc.identifier.scopuseid_2-s2.0-79251629978
 
dc.identifier.spage643
 
dc.identifier.urihttp://hdl.handle.net/10722/138935
 
dc.identifier.volume112
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Cellular Biochemistry
 
dc.relation.referencesReferences in Scopus
 
dc.rightsJournal of Cellular Biochemistry. Copyright © John Wiley & Sons, Inc.
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshColonic Neoplasms - genetics - metabolism
 
dc.subject.meshMediator Complex - genetics
 
dc.subject.meshPhloroglucinol - analogs and derivatives - pharmacology
 
dc.subject.meshTranscription Factor CHOP/genetics
 
dc.titlePhloroglucinol derivative MCPP induces cell apoptosis in human colon cancer
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Huang, SM</contributor.author>
<contributor.author>Cheung, CW</contributor.author>
<contributor.author>Chang, CS</contributor.author>
<contributor.author>Tang, CH</contributor.author>
<contributor.author>Liu, JF</contributor.author>
<contributor.author>Lin, YH</contributor.author>
<contributor.author>Chen, JH</contributor.author>
<contributor.author>Ko, SH</contributor.author>
<contributor.author>Wong, KL</contributor.author>
<contributor.author>Lu, DY</contributor.author>
<date.accessioned>2011-09-23T05:42:19Z</date.accessioned>
<date.available>2011-09-23T05:42:19Z</date.available>
<date.issued>2011</date.issued>
<identifier.citation>Journal of Cellular Biochemistry, 2011, v. 112 n. 2, p. 643-652</identifier.citation>
<identifier.issn>0730-2312</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/138935</identifier.uri>
<description.abstract>This study is the first to investigate the anticancer effects of the new phloroglucinol derivative (3,6-bis(3-chlorophenylacetyl)phloroglucinol; MCPP) in human colon cancer cells. MCPP induced cell death and antiproliferation in three human colon cancer, HCT-116, SW480, and Caco-2 cells, but not in primary human dermal fibroblast cells. MCPP-induced concentration-dependent apoptotic cell death in colon cancer cells was measured by fluorescence-activated cell sorter (FACS) analysis. Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2alpha (eIF-2alpha), suggesting the induction of ER stress. MCPP also increased GSK3alpha/beta(Tyr270/216) phosphorylation and reduced GSK3alpha/beta(Ser21/9) phosphorylation time-dependently. Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP-mediated cell apoptosis. Treatment of MCPP also increased caspase-7, caspase-9, and caspase-3 activity. The inhibition of caspase activity by z-DEVE-FMK or z-VAD-FMK significantly reduced MCPP-induced apoptosis. Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation. Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3alpha/beta activation in mediating the MCPP-induced human colon cancer cell apoptosis. &#169; 2010 Wiley-Liss, Inc.</description.abstract>
<language>eng</language>
<publisher>John Wiley &amp; Sons, Inc. The Journal&apos;s web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503</publisher>
<relation.ispartof>Journal of Cellular Biochemistry</relation.ispartof>
<rights>Journal of Cellular Biochemistry. Copyright &#169; John Wiley &amp; Sons, Inc.</rights>
<subject.mesh>Cell Line, Tumor</subject.mesh>
<subject.mesh>Colonic Neoplasms - genetics - metabolism</subject.mesh>
<subject.mesh>Mediator Complex - genetics</subject.mesh>
<subject.mesh>Phloroglucinol - analogs and derivatives - pharmacology</subject.mesh>
<subject.mesh>Transcription Factor CHOP/genetics</subject.mesh>
<title>Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer</title>
<type>Article</type>
<description.nature>Link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1002/jcb.22966</identifier.doi>
<identifier.pmid>21268086</identifier.pmid>
<identifier.scopus>eid_2-s2.0-79251629978</identifier.scopus>
<identifier.hkuros>193530</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-79251629978&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>112</identifier.volume>
<identifier.issue>2</identifier.issue>
<identifier.spage>643</identifier.spage>
<identifier.epage>652</identifier.epage>
<identifier.isi>WOS:000287071900033</identifier.isi>
<publisher.place>United States</publisher.place>
</item>
Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. null
  3. China Medical University Hospital Taichung
  4. Buddhist Tzu-Chi General Hospital Taiwan