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Article: Prostate cancer cells modulate osteoblast mineralisation and osteoclast differentiation through Id-1

TitleProstate cancer cells modulate osteoblast mineralisation and osteoclast differentiation through Id-1
Authors
KeywordsBone metastasis
Id-1
Osteoblast
Osteoclast
Prostate cancer
Issue Date2010
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
Citation
British Journal Of Cancer, 2010, v. 102 n. 2, p. 332-341 How to Cite?
AbstractBackground: Id-1 is overexpressed in and correlated with metastatic potential of prostate cancer. The role of Id-1 in this metastatic process was further analysed. Methods: Conditioned media from prostate cancer cells, expressing various levels of Id-1, were used to stimulate pre-osteoclast differentiation and osteoblast mineralisation. Downstream effectors of Id-1 were identified. Expressions of Id-1 and its downstream effectors in prostate cancers were studied using immunohistochemistry in a prostate cancer patient cohort (N110). Results: We found that conditioned media from LNCaP prostate cancer cells overexpressing Id-1 had a higher ability to drive osteoclast differentiation and a lower ability to stimulate osteoblast mineralisation than control, whereas conditioned media from PC3 prostate cancer cells with Id-1 knockdown were less able to stimulate osteoclast differentiation. Id-1 was found to negatively regulate TNF-Β and this correlation was confirmed in human prostate cancer specimens (P0.03). Furthermore, addition of recombinant TNF-Β to LNCaP Id-1 cell-derived media blocked the effect of Id-1 overexpression on osteoblast mineralisation. Conclusion: In prostate cancer cells, the ability of Id-1 to modulate bone cell differentiation favouring metastatic bone disease is partially mediated by TNF-Β, and Id-1 could be a potential therapeutic target for prostate cancer to bone metastasis. © 2010 Cancer Research UK. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/126700
ISSN
2015 Impact Factor: 5.569
2015 SCImago Journal Rankings: 2.939
ISI Accession Number ID
Funding AgencyGrant Number
Cancer Research UK
Funding Information:

We thank Dr MT Ling for his technical support in creating the LNCaP and PC-3 cell line derivatives and also Cancer Research UK for the post-doctoral fellowship to HF Yuen.

References

 

DC FieldValueLanguage
dc.contributor.authorYuen, HFen_HK
dc.contributor.authorChiu, YTen_HK
dc.contributor.authorChan, KKen_HK
dc.contributor.authorChan, YPen_HK
dc.contributor.authorChua, CWen_HK
dc.contributor.authorMcCrudden, CMen_HK
dc.contributor.authorTang, KHen_HK
dc.contributor.authorElTanani, Men_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorChan, KWen_HK
dc.date.accessioned2010-10-31T12:43:28Z-
dc.date.available2010-10-31T12:43:28Z-
dc.date.issued2010en_HK
dc.identifier.citationBritish Journal Of Cancer, 2010, v. 102 n. 2, p. 332-341en_HK
dc.identifier.issn0007-0920en_HK
dc.identifier.urihttp://hdl.handle.net/10722/126700-
dc.description.abstractBackground: Id-1 is overexpressed in and correlated with metastatic potential of prostate cancer. The role of Id-1 in this metastatic process was further analysed. Methods: Conditioned media from prostate cancer cells, expressing various levels of Id-1, were used to stimulate pre-osteoclast differentiation and osteoblast mineralisation. Downstream effectors of Id-1 were identified. Expressions of Id-1 and its downstream effectors in prostate cancers were studied using immunohistochemistry in a prostate cancer patient cohort (N110). Results: We found that conditioned media from LNCaP prostate cancer cells overexpressing Id-1 had a higher ability to drive osteoclast differentiation and a lower ability to stimulate osteoblast mineralisation than control, whereas conditioned media from PC3 prostate cancer cells with Id-1 knockdown were less able to stimulate osteoclast differentiation. Id-1 was found to negatively regulate TNF-Β and this correlation was confirmed in human prostate cancer specimens (P0.03). Furthermore, addition of recombinant TNF-Β to LNCaP Id-1 cell-derived media blocked the effect of Id-1 overexpression on osteoblast mineralisation. Conclusion: In prostate cancer cells, the ability of Id-1 to modulate bone cell differentiation favouring metastatic bone disease is partially mediated by TNF-Β, and Id-1 could be a potential therapeutic target for prostate cancer to bone metastasis. © 2010 Cancer Research UK. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjcen_HK
dc.relation.ispartofBritish Journal of Canceren_HK
dc.subjectBone metastasisen_HK
dc.subjectId-1en_HK
dc.subjectOsteoblasten_HK
dc.subjectOsteoclasten_HK
dc.subjectProstate canceren_HK
dc.subject.meshCalcification, Physiologic - physiologyen_HK
dc.subject.meshCell Differentiationen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshHumansen_HK
dc.subject.meshInhibitor of Differentiation Protein 1 - biosynthesisen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNeoplasm Metastasisen_HK
dc.subject.meshOsteoblasts - metabolismen_HK
dc.subject.meshOsteoclasts - metabolismen_HK
dc.subject.meshOsteogenesis - physiologyen_HK
dc.subject.meshProstatic Neoplasmsen_HK
dc.titleProstate cancer cells modulate osteoblast mineralisation and osteoclast differentiation through Id-1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-0920&volume=102&spage=332&epage=341&date=2010&atitle=Prostate+Cancer+Cells+Modulate+Osteoblast+Mineralisation+And+Osteoclast+Differentiation+Through+Id-1en_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_OA_fulltext-
dc.identifier.doi10.1038/sj.bjc.6605480en_HK
dc.identifier.pmid20010941-
dc.identifier.scopuseid_2-s2.0-75549090864en_HK
dc.identifier.hkuros178833en_HK
dc.identifier.hkuros218578-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-75549090864&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume102en_HK
dc.identifier.issue2en_HK
dc.identifier.spage332en_HK
dc.identifier.epage341en_HK
dc.identifier.isiWOS:000273728500013-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYuen, HF=14018633400en_HK
dc.identifier.scopusauthoridChiu, YT=23975797700en_HK
dc.identifier.scopusauthoridChan, KK=8986914100en_HK
dc.identifier.scopusauthoridChan, YP=14009821700en_HK
dc.identifier.scopusauthoridChua, CW=9437494600en_HK
dc.identifier.scopusauthoridMcCrudden, CM=16402813600en_HK
dc.identifier.scopusauthoridTang, KH=24781597200en_HK
dc.identifier.scopusauthoridElTanani, M=6602759648en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridWang, X=9249338400en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.citeulike6431612-

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