Dr Hong Wan, BDS, MSc, PhD, FHEA
Non-Clinical Senior Lecturer in Cell Biology
Email: firstname.lastname@example.orgTelephone: +44 (0) 207 882 7139Room Number: Blizard Building
1978-83 BDS, School of Stomatology, West China University of Medical Sciences, Sichuan University, China.
1983-85 General Dentist, Zhongshan Hospital, Shanghai First Medical University, Shanghai, China.
1985-88 MSc in Prosthodontics, School of Stomatology, West China University of Medical Sciences, Sichuan University, China.
1988-91 Lecturer in Prosthetic Department, School of Stomatology, West China University of Medical Sciences, Sichuan University, China.
1991-95 PhD in Department of Clinical Engineering, University of Liverpool.
1996-99 Postdoctoral research fellow (Wellcome Trust funded), St. George’s Hospital Medical School, University of London.
1999-2003 Postdoctoral research associate (Wellcome Trust funded), St. John’s Institute of Dermatology, St Thomas’ Hospital, UK.
2004-2006 MRC fellow (funded by a MRC Career Development Fellowship for Stem Cell Research), Tumour Biology, Barts Cancer Institute, Barts and The London School of Medicine and Dentistry, QMUL.
2007-present Non-clinical senior lecturer, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, QMUL.
Giving lectures / seminars to the 1st year BDS undergraduates, postgraduates of MSc Experimental Oral Pathology, and biomedical life science students, on topics in biochemistry, histology, membrane biology, cell adhesion and migration, research in vesiculobullous diseases.
Teaching students on MSc Experimental Oral Pathology on the lab practical in immunofluorescence and western blotting.
Supervising 3rd year BDS students on SSC and students of SBS 206 Project Skills in the Life Sciences on the dissertations.
Dr Wan’s research focuses on cell-cell junctions in health and disease. Cell-cell junctions are multiprotein adhesion complexes located on the plasma membrane of the cell and play an essential role in cell adhesion and the maintenance of tissue integrity. These junctions crosstalk one another and coordinate with a diversity of cellular processes such as proliferation, differentiation, morphogenesis, as well as cell motility. Alterations of these junctions can lead to a broad spectrum of human diseases, including cancer and vesiculobullous conditions. Increasing evidence indicates that many components of these junctions also participate in cell signalling and are acting as sensors to the environmental biochemical and mechanical cues.
Her recent studies have identified Desmoglein-3 (Dsg3) acting as an anti-stress protein via regulating the mechanosensor YAP, cancer suppressor p53, as well as AP-1 transcription factor, that have a direct impact on the cell fate decision. These findings underscore the unprecedented role of Dsg3 in the control of higher-ordered network essential for tissue regeneration and homeostasis beyond cell-cell adhesion. Elucidation of the underlying molecular basis is crucial to understand the pathogenesis of the associated disorders such as cancer and pemphigus autoimmune disease in which Dsg3 is altered.
Dr Wan’s research approach is mainly based on in vitro studies with both gain and loss of function strategies in conjunction with the pharmacological interventions in keratinocyte cells derived from both the skin and oral mucosal membrane. The ultimate goal of her research is to translate the significant findings to clinical research to improve the diagnosis and treatment of related diseases.
1. Uttagomol J, Ahmad US, Rehman A, Huang Y, Laly AC, Kang A, Soetaert J, Chance R, Muy-Teck Teh, John T. Connelly and Wan H. Evidence for the desmosomal cadherin desmoglein-3 in regulating YAP and Phospho-YAP in keratinocyte responses to mechanical forces. Int J Mol Sci, 2019; Dec 10;20(24):6221
2. Rehman A, Cai Y, Hünefeld C, Jedličková H, Huang Y, Teck Teh M, Sharif Ahmad U, Uttagomol J, Wang Y, Kang A, Warnes G, Harwood C, Bergamaschi D, Kenneth Parkinson E, Röcken M, and Wan H. The desmosomal cadherin desmoglein-3 acts as a keratinocyte anti-stress protein via suppression of p53. Cell Death Dis, 2019; Oct 3;10(10):750
3. Brown L, Waseem A, Cruz IN, Szary J, Gunic E, Mannan T, Unadkat M, Yang M, F Valderrama, E A O′Toole and H Wan. Desmoglein 3 promotes cancer cell migration and invasion by regulating activator protein 1 and protein kinase C-dependent-Ezrin activation. Oncogene, 2013; vol. 33, 2363-237
4. Tsang SM, Brown L, Lin K, Liu L, Piper K, O'Toole EA, Grose R, Hart IR, David R Garrod, Farida Fortune, Hong Wan. Non-junctional human desmoglein 3 acts as an upstream regulator of Src in E-cadherin adhesion, a pathway possibly involved in the pathogenesis of pemphigus vulgaris. J Pathol, 2012; vol. 227, (1) 81-93
5. Tsang SM, Liu L, Teh M-T, Wheeler A, Grose R, Hart IR, Garrod DR, Fortune F and Wan H. Desmoglein 3, via an interaction with E-cadherin, is associated with activation of Src. PloS ONE, 2010; vol. 5, (12)
Supervising the project research students at all levels, including PhD, MSc Experimental Oral Pathology / Regenerative Medicine, iBSc Oral Biology.
So far I have successfully supervised 7 PhDs and more than 22 MSc / iBSc students.