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Article: Tie-2 regulates the stemness and metastatic properties of prostate cancer cells.

TitleTie-2 regulates the stemness and metastatic properties of prostate cancer cells.
Authors
Issue Date2016
PublisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html
Citation
Oncotarget, 2016, v. 7 n. 3, p. 2572-2584 How to Cite?
AbstractAmple evidence supports that prostate tumor metastasis originates from a rare population of cancer cells, known as cancer stem cells (CSCs). Unfortunately, little is known about the identity of these cells, making it difficult to target the metastatic prostate tumor. Here, for the first time, we report the identification of a rare population of prostate cancer cells that express the Tie-2 protein. We found that this Tie-2High population exists mainly in prostate cancer cell lines that are capable of metastasizing to the bone. These cells not only express a higher level of CSC markers but also demonstrate enhanced resistance to the chemotherapeutic drug Cabazitaxel. In addition, knockdown of the expression of the Tie-2 ligand angiopoietin (Ang-1) led to suppression of CSC markers, suggesting that the Ang-1/Tie-2 signaling pathway functions as an autocrine loop for the maintenance of prostate CSCs. More importantly, we found that Tie-2High prostate cancer cells are more adhesive than the Tie-2Low population to both osteoblasts and endothelial cells. Moreover, only the Tie-2High, but not the Tie-2Low cells developed tumor metastasis in vivo when injected at a low number. Taken together, our data suggest that Tie-2 may play an important role during the development of prostate tumor metastasis.
Persistent Identifierhttp://hdl.handle.net/10722/215078
ISSN
2015 Impact Factor: 5.008
2015 SCImago Journal Rankings: 2.294

 

DC FieldValueLanguage
dc.contributor.authorTang, KD-
dc.contributor.authorHolzapfel, BM-
dc.contributor.authorLiu, J-
dc.contributor.authorLee, TKW-
dc.contributor.authorMa, SKY-
dc.contributor.authorJovanovix, L-
dc.contributor.authorAn, J-
dc.contributor.authorRussell, PJ-
dc.contributor.authorClements, JA-
dc.contributor.authorHutmacher, DW-
dc.contributor.authorLing, MT-
dc.date.accessioned2015-08-21T12:25:08Z-
dc.date.available2015-08-21T12:25:08Z-
dc.date.issued2016-
dc.identifier.citationOncotarget, 2016, v. 7 n. 3, p. 2572-2584-
dc.identifier.issn1949-2553-
dc.identifier.urihttp://hdl.handle.net/10722/215078-
dc.description.abstractAmple evidence supports that prostate tumor metastasis originates from a rare population of cancer cells, known as cancer stem cells (CSCs). Unfortunately, little is known about the identity of these cells, making it difficult to target the metastatic prostate tumor. Here, for the first time, we report the identification of a rare population of prostate cancer cells that express the Tie-2 protein. We found that this Tie-2High population exists mainly in prostate cancer cell lines that are capable of metastasizing to the bone. These cells not only express a higher level of CSC markers but also demonstrate enhanced resistance to the chemotherapeutic drug Cabazitaxel. In addition, knockdown of the expression of the Tie-2 ligand angiopoietin (Ang-1) led to suppression of CSC markers, suggesting that the Ang-1/Tie-2 signaling pathway functions as an autocrine loop for the maintenance of prostate CSCs. More importantly, we found that Tie-2High prostate cancer cells are more adhesive than the Tie-2Low population to both osteoblasts and endothelial cells. Moreover, only the Tie-2High, but not the Tie-2Low cells developed tumor metastasis in vivo when injected at a low number. Taken together, our data suggest that Tie-2 may play an important role during the development of prostate tumor metastasis.-
dc.languageeng-
dc.publisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html-
dc.relation.ispartofOncotarget-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleTie-2 regulates the stemness and metastatic properties of prostate cancer cells.-
dc.typeArticle-
dc.identifier.emailLee, TKW: tkwlee@hkucc.hku.hk-
dc.identifier.emailMa, SKY: stefma@hku.hk-
dc.identifier.authorityLee, TKW=rp00447-
dc.identifier.authorityMa, SKY=rp00506-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.18632/oncotarget.3950-
dc.identifier.pmid25200314-
dc.identifier.hkuros247000-
dc.identifier.volume7-
dc.identifier.issue3-
dc.identifier.spage2572-
dc.identifier.epage2584-
dc.publisher.placeUnited States-

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