电脑辅助及远程认知康复的发展与应用

2003-2004 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Feasibility investigation of cognitive rehabilitation service after traumatic brain injury in community

2003-2004 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Efficient immortalization of primary nasopharyngeal epithelial cells for EBV infection study

Author name used in this publication: Cornelia Man2013-2014 > Academic research: refereed > Publication in refereed journalpublished_fina

Id1 overexpression induces tetraploidization and multiple abnormal mitotic phenotypes by modulating aurora A.

Session - Cancer 3 (2168 – 2195): abstract no. 2187/B656The basic helix-loop-helix transcription factor, Id1, was shown to induce tetraploidy in telomerase-immortalized nasopharyngeal epithelial cells in this study. Using both transient and stable Id1-expressing cell models, multiple mitotic aberrations were detected; including centrosome amplification, binucleation, spindle defects and microtubule perturbation. Many of these abnormal phenotypes have previously been reported in cells overexpressing Aurora A. Further experiments showed that Id1 could stabilize Aurora A, while knocking down Aurora A expression in Id1-expressing cells could rescue some of the mitotic defects. The mechanisms by which Aurora A could be modulated by Id1 were explored. DNA amplification of the Aurora A locus was not involved. Id1 could only weakly activate the transcriptional activity of the Aurora A promoter. We found that Id1 overexpression could affect Aurora A degradation, leading to its stabilization. Aurora A is normally degraded from mitosis exit by the APC/C Cdh1-mediated proteasomal proteolysis pathway. Our results revealed that Id1 and Cdh1 are binding partners. The association of Id1 and Cdh1 was found to be dependent on the canonical destruction box (D box) motif of Id1; the increased binding of which may compete with the interaction between cdh1 and Aurora A, leading to stabilization of Aurora A in Id1-overexpressing cells.link_to_OA_fulltex

Differential ERα-mediated rapid estrogenic actions of ginsenoside Rg1 and estren in human breast cancer MCF-7 cells

2013-2014 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptRGCPolyU 5632/11MPublishe

Functional study of the EBV encoded LMP1

The Epstein-Barr virus encoded LMP1 is expressed in nasopharyngeal caricinoma cells. Recently, we have showed that LMP1 expression in immortalized epithelial cells could induce mitotic abnormality by downregulating RASSF1A expression. Downregulation of RASSF1A affects the stability of microtubules and induces formation of abnormal spindle. Expression of LMP1 could induce many pathologic phenotypes in cells. Expression of LMP1 induces upregulation of IL6 expression to activate STAT3 signaling which may mediate the pathologic properties of nasopharyngeal carcinoma cells. LMP1 expression in immortalized nasopharyngeal epithelial cells induces malignantly transformated phenotype including anchorage independent growth in soft agar, increase of invasive properties and activation of intracellular signaling for cell survival and anti-apoptosis. LMP1 expression also suppresses the exprssion of squamous differentitation marker, p63 and other differentation properties in immortalized epithelial cells. Recently, we have showed that LMP1 could also facilitate immortalization of primary cultures of nasopharyngeal epithelial cells. LMP1 immortalized nasopharyngeal epithelial cells have upregulated MAPK signaling pathways and overexpression of EGFR