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Article: TWIST modulates prostate cancer cell-mediated bone cell activity and is upregulated by osteogenic induction

TitleTWIST modulates prostate cancer cell-mediated bone cell activity and is upregulated by osteogenic induction
Authors
Issue Date2008
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2008, v. 29 n. 8, p. 1509-1518 How to Cite?
AbstractTWIST, a helix-loop-helix transcription factor, is highly expressed in many types of human cancer. We have previously found that TWIST confers prostate cancer cells with an enhanced metastatic potential through promoting epithelial-mesenchymal transition (EMT) and a high TWIST expression in human prostate cancer is associated with an increased metastatic potential. The predilection of prostate cancer cells to metastasize to bone may be due to two interplaying mechanisms (i) by increasing the rate of bone remodeling and (ii) by undergoing osteomimicry. We further studied the role of TWIST in promoting prostate cancer to bone metastasis. TWIST expression in PC3, a metastatic prostate cancer cell line, was silenced by small interfering RNA and we found that conditioned medium from PC3 with lower TWIST expression had a lower activity on stimulating osteoclast differentiation and higher activity on stimulating osteoblast mineralization. In addition, we found that these effects were, at least partly, associated with TWIST-induced expression of dickkopf homolog 1 (DKK-1), a factor that promotes osteolytic metastasis. We also examined TWIST and RUNX2 expressions during osteogenic induction of an organ-confined prostate cancer cell, 22Rv1. We observed increased TWIST and RUNX2 expressions upon osteogenic induction and downregulation of TWIST through short hairpin RNA reduced the induction level of RUNX2. In summary, our results suggest that, in addition to EMT, TWIST may also promote prostate cancer to bone metastasis by modulating prostate cancer cell-mediated bone remodeling via regulating the expression of a secretory factor, DKK-1, and enhancing osteomimicry of prostate cancer cells, probably, via RUNX2. © The Author 2008. Published by Oxford University Press. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/58207
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuen, HFen_HK
dc.contributor.authorKwok, WKen_HK
dc.contributor.authorChan, KKen_HK
dc.contributor.authorChua, CWen_HK
dc.contributor.authorChan, YPen_HK
dc.contributor.authorChu, YYen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorChan, KWen_HK
dc.date.accessioned2010-05-31T03:25:50Z-
dc.date.available2010-05-31T03:25:50Z-
dc.date.issued2008en_HK
dc.identifier.citationCarcinogenesis, 2008, v. 29 n. 8, p. 1509-1518en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58207-
dc.description.abstractTWIST, a helix-loop-helix transcription factor, is highly expressed in many types of human cancer. We have previously found that TWIST confers prostate cancer cells with an enhanced metastatic potential through promoting epithelial-mesenchymal transition (EMT) and a high TWIST expression in human prostate cancer is associated with an increased metastatic potential. The predilection of prostate cancer cells to metastasize to bone may be due to two interplaying mechanisms (i) by increasing the rate of bone remodeling and (ii) by undergoing osteomimicry. We further studied the role of TWIST in promoting prostate cancer to bone metastasis. TWIST expression in PC3, a metastatic prostate cancer cell line, was silenced by small interfering RNA and we found that conditioned medium from PC3 with lower TWIST expression had a lower activity on stimulating osteoclast differentiation and higher activity on stimulating osteoblast mineralization. In addition, we found that these effects were, at least partly, associated with TWIST-induced expression of dickkopf homolog 1 (DKK-1), a factor that promotes osteolytic metastasis. We also examined TWIST and RUNX2 expressions during osteogenic induction of an organ-confined prostate cancer cell, 22Rv1. We observed increased TWIST and RUNX2 expressions upon osteogenic induction and downregulation of TWIST through short hairpin RNA reduced the induction level of RUNX2. In summary, our results suggest that, in addition to EMT, TWIST may also promote prostate cancer to bone metastasis by modulating prostate cancer cell-mediated bone remodeling via regulating the expression of a secretory factor, DKK-1, and enhancing osteomimicry of prostate cancer cells, probably, via RUNX2. © The Author 2008. Published by Oxford University Press. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsCarcinogenesis. Copyright © Lippincott Williams & Wilkins.en_HK
dc.subject.mesh3T3 Cellsen_HK
dc.subject.meshAlkaline Phosphatase - metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBone Neoplasms - secondaryen_HK
dc.subject.meshBone and Bones - physiopathologyen_HK
dc.subject.meshCalcification, Physiologicen_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCore Binding Factor Alpha 1 Subunit - geneticsen_HK
dc.subject.meshDNA Primersen_HK
dc.subject.meshGenes, Reporteren_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshNuclear Proteins - geneticsen_HK
dc.subject.meshOsteoblasts - cytology - physiologyen_HK
dc.subject.meshOsteogenesis - physiologyen_HK
dc.subject.meshPlasmidsen_HK
dc.subject.meshProstatic Neoplasms - pathologyen_HK
dc.subject.meshRNA, Small Interfering - geneticsen_HK
dc.subject.meshTwist Transcription Factor - geneticsen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleTWIST modulates prostate cancer cell-mediated bone cell activity and is upregulated by osteogenic inductionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0147-4006&volume=29&issue=8&spage=1509&epage=18&date=2008&atitle=TWIST+modulates+prostate+cancer+cell-mediated+bone+cell+activity+and+is+upregulated+by+osteogenic+inductionen_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailChan, KW:hrmtckw@hku.hken_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/carcin/bgn105en_HK
dc.identifier.pmid18453541-
dc.identifier.scopuseid_2-s2.0-49649097767en_HK
dc.identifier.hkuros159781en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-49649097767&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1509en_HK
dc.identifier.epage1518en_HK
dc.identifier.isiWOS:000258471900006-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYuen, HF=14018633400en_HK
dc.identifier.scopusauthoridKwok, WK=8578541800en_HK
dc.identifier.scopusauthoridChan, KK=8986914100en_HK
dc.identifier.scopusauthoridChua, CW=9437494600en_HK
dc.identifier.scopusauthoridChan, YP=14009821700en_HK
dc.identifier.scopusauthoridChu, YY=22984019500en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK

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