Please use this identifier to cite or link to this item:
https://doi.org/10.1002/emmm.201202183
DC Field | Value | |
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dc.title | Oncogenic roles of PRL-3 in FLT3-ITD induced acute myeloid leukaemia | |
dc.contributor.author | Park, J.E. | |
dc.contributor.author | Yuen, H.F. | |
dc.contributor.author | Zhou, J.B. | |
dc.contributor.author | Al-aidaroos, A.Q.O. | |
dc.contributor.author | Guo, K. | |
dc.contributor.author | Valk, P.J. | |
dc.contributor.author | Zhang, S.D. | |
dc.contributor.author | Chng, W.J. | |
dc.contributor.author | Hong, C.W. | |
dc.contributor.author | Mills, K. | |
dc.contributor.author | Zeng, Q. | |
dc.date.accessioned | 2014-12-12T08:01:36Z | |
dc.date.available | 2014-12-12T08:01:36Z | |
dc.date.issued | 2013-09 | |
dc.identifier.citation | Park, J.E., Yuen, H.F., Zhou, J.B., Al-aidaroos, A.Q.O., Guo, K., Valk, P.J., Zhang, S.D., Chng, W.J., Hong, C.W., Mills, K., Zeng, Q. (2013-09). Oncogenic roles of PRL-3 in FLT3-ITD induced acute myeloid leukaemia. EMBO Molecular Medicine 5 (9) : 1351-1366. ScholarBank@NUS Repository. https://doi.org/10.1002/emmm.201202183 | |
dc.identifier.issn | 17574676 | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/117106 | |
dc.description.abstract | FLT3-ITD mutations are prevalent mutations in acute myeloid leukaemia (AML). PRL-3, a metastasis-associated phosphatase, is a downstream target of FLT3-ITD. This study investigates the regulation and function of PRL-3 in leukaemia cell lines and AML patients associated with FLT3-ITD mutations. PRL-3 expression is upregulated by the FLT3-STAT5 signalling pathway in leukaemia cells, leading an activation of AP-1 transcription factors via ERK and JNK pathways. PRL-3-depleted AML cells showed a significant decrease in cell growth. Clinically, high PRL-3 mRNA expression was associated with FLT3-ITD mutations in four independent AML datasets with 1158 patients. Multivariable Cox-regression analysis on our Cohort 1 with 221 patients identified PRL-3 as a novel prognostic marker independent of other clinical parameters. Kaplan-Meier analysis showed high PRL-3 mRNA expression was significantly associated with poorer survival among 491 patients with normal karyotype. Targeting PRL-3 reversed the oncogenic effects in FLT3-ITD AML models in vitro and in vivo. Herein, we suggest that PRL-3 could serve as a prognostic marker to predict poorer survival and as a promising novel therapeutic target for AML patients. © 2013 The Authors. Published by John Wiley and Sons, Ltd on behalf of EMBO. | |
dc.description.uri | http://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1002/emmm.201202183 | |
dc.source | Scopus | |
dc.subject | Acute myeloid leukaemia | |
dc.subject | Antibody therapy | |
dc.subject | FLT3-ITD mutation | |
dc.subject | PRL-3 | |
dc.subject | Prognostic marker | |
dc.type | Article | |
dc.contributor.department | CANCER SCIENCE INSTITUTE OF SINGAPORE | |
dc.contributor.department | INSTITUTE OF MOLECULAR & CELL BIOLOGY | |
dc.description.doi | 10.1002/emmm.201202183 | |
dc.description.sourcetitle | EMBO Molecular Medicine | |
dc.description.volume | 5 | |
dc.description.issue | 9 | |
dc.description.page | 1351-1366 | |
dc.identifier.isiut | 000323783000007 | |
Appears in Collections: | Staff Publications |
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