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Article: Proline-rich acidic protein 1 (PRAP1) is a novel interacting partner of MAD1 and has a suppressive role in mitotic checkpoint signalling in hepatocellular carcinoma.

TitleProline-rich acidic protein 1 (PRAP1) is a novel interacting partner of MAD1 and has a suppressive role in mitotic checkpoint signalling in hepatocellular carcinoma.
Authors
Issue Date2014
PublisherJohn Wiley & Sons, Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130
Citation
Journal of Pathology, 2014, v. 233 n. 1, p. 51-60 How to Cite?
AbstractLoss of mitotic checkpoint of cells contributes to chromosomal instability and leads to carcinogenesis. Mitotic arrest deficient 1 (MAD1) is a key component in mitotic checkpoint signalling. In this study, we identified a novel MAD1 interacting partner, proline-rich acidic protein 1 (PRAP1), using yeast-two hybrid screening, and investigated its role in mitotic checkpoint signalling in hepatocellular carcinoma (HCC). We demonstrated the physical interaction of PRAP1 with MAD1 and of PRAP1 with MAD1 isoform MAD1β, using a co-immunoprecipitation assay. Moreover, stable expression of PRAP1 in mitotic checkpoint-competent HCC cells, BEL-7402 and SMMC-7721, induced impairment of the mitotic checkpoint (p < 0.01), formation of chromosome bridges (p < 0.01) and aberrant chromosome numbers (p < 0.001). Interestingly, ectopic expression PRAP1 in HCC cells led to significant under-expression of MAD1. In human HCC tumours, 40.4% (23/57) of HCCs showed under-expression of PRAP1 protein as compared with their corresponding non-tumorous livers; up-regulation of MAD1 protein was significantly associated with down-regulation of PRAP1 (p = 0.030). Our data revealed that PRAP1 is a protein interacting partner of MAD1 and that PRAP1 is able to down-regulate MAD1 and suppress mitotic checkpoint signalling in HCC.
Persistent Identifierhttp://hdl.handle.net/10722/199301

 

DC FieldValueLanguage
dc.contributor.authorSze, MFen_US
dc.contributor.authorChu, KYen_US
dc.contributor.authorMak, HYen_US
dc.contributor.authorLee, MFen_US
dc.contributor.authorNg, IOLen_US
dc.date.accessioned2014-07-22T01:12:22Z-
dc.date.available2014-07-22T01:12:22Z-
dc.date.issued2014en_US
dc.identifier.citationJournal of Pathology, 2014, v. 233 n. 1, p. 51-60en_US
dc.identifier.urihttp://hdl.handle.net/10722/199301-
dc.description.abstractLoss of mitotic checkpoint of cells contributes to chromosomal instability and leads to carcinogenesis. Mitotic arrest deficient 1 (MAD1) is a key component in mitotic checkpoint signalling. In this study, we identified a novel MAD1 interacting partner, proline-rich acidic protein 1 (PRAP1), using yeast-two hybrid screening, and investigated its role in mitotic checkpoint signalling in hepatocellular carcinoma (HCC). We demonstrated the physical interaction of PRAP1 with MAD1 and of PRAP1 with MAD1 isoform MAD1β, using a co-immunoprecipitation assay. Moreover, stable expression of PRAP1 in mitotic checkpoint-competent HCC cells, BEL-7402 and SMMC-7721, induced impairment of the mitotic checkpoint (p < 0.01), formation of chromosome bridges (p < 0.01) and aberrant chromosome numbers (p < 0.001). Interestingly, ectopic expression PRAP1 in HCC cells led to significant under-expression of MAD1. In human HCC tumours, 40.4% (23/57) of HCCs showed under-expression of PRAP1 protein as compared with their corresponding non-tumorous livers; up-regulation of MAD1 protein was significantly associated with down-regulation of PRAP1 (p = 0.030). Our data revealed that PRAP1 is a protein interacting partner of MAD1 and that PRAP1 is able to down-regulate MAD1 and suppress mitotic checkpoint signalling in HCC.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130en_US
dc.relation.ispartofJournal of Pathologyen_US
dc.titleProline-rich acidic protein 1 (PRAP1) is a novel interacting partner of MAD1 and has a suppressive role in mitotic checkpoint signalling in hepatocellular carcinoma.en_US
dc.typeArticleen_US
dc.identifier.emailSze, MF: karensze@hkucc.hku.hken_US
dc.identifier.emailChu, KY: glanice@hku.hken_US
dc.identifier.emailLee, MF: joyce@pathology.hku.hken_US
dc.identifier.emailNg, IOL: iolng@hku.hken_US
dc.identifier.doi10.1002/path.4319-
dc.identifier.hkuros230973en_US
dc.identifier.volume233en_US
dc.identifier.issue1en_US
dc.identifier.spage51en_US
dc.identifier.epage60en_US
dc.publisher.placeGreat Britain and Irelanden_US

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