Dr Yihua Wang is Lecturer in Biomedical Sciences within the School of Biological Sciences at the University of Southampton.
Career History
2009-2015: Postdoctoral Molecular Biologist. Ludwig Institute for Cancer Research, University of Oxford, UK. 2006-2009: Research Fellow. Cancer Research UK, London Research Institute, London, UK.
Academic Qualifications
2018: Postgraduate Certificate in Academic Practice. 2017: Fellow of The Higher Education Academy. 2006: PhD Cell Biology. Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China. 2001: MBBS. Tongji Medical University, Wuhan, China.
Research
Responsibilities
Publications
Teaching
Contributions
Contact
Research interests
I have a long held interest in functional genomics and cell signaling. My postdoctoral work helped define several mechanisms that govern the activity of RAS signaling and epithelial-mesenchymal transition (EMT) - the shift from a highly structured epithelial state to a flexible and motile mesenchymal form. These studies led me to appreciate the complexity of cell signaling required to control the plasticity of epithelial cells, which plays critical roles in a number of biological phenomena, including embryonic development, tissue repair, organ fibrosis and, not least, tumour metastasis.
EMT requires complex orchestration of multiple signaling pathways, including RAS pathway, which has been implicated in cancer as well as in idiopathic pulmonary fibrosis (IPF), a chronic, progressive, irreversible, and usually lethal lung disease characterized by interstitial fibrosis of unknown pathogenesis. Although IPF has been considered rare, it occurs with similar frequency to that of stomach, brain, and testicular cancers. Alveolar Type II (ATII) epithelial cells function as stem cells, contributing to alveolar renewal, repair and cancer. Therefore, they are a highly relevant model for studying pathologic EMT, especially considering the high burden of lung diseases, including acute lung injury, lung fibrosis and lung cancer. Using 3D culture of ATII cells, RNAi screen and proteomics, I aim to identify drug targets or biomarkers to intervene or predict the progression of RAS-mutated cancer and IPF.
My laboratory interacts and collaborates with many researchers across different disciplines at the Southampton Institute for Life Sciences and the Southampton Faculty of Medicine, as well as scientists in the Francis Crick Institute.
Current grants:
Royal Society's Research Grants.
Wessex Medical Research Innovation Grant.
The Academy of Medical Sciences/ the Wellcome Trust Springboard
Asthma Allergy & Inflammation Research Trust Research Award
MRC New Investigator Research Grant
Most recent publications:
Hill C, Li J, Liu D, Conforti F, Brereton CJ, Yao L, Zhou Y, Alzetani A, Chee SJ, Marshall BG, Fletcher SV, Hancock D, Ottensmeier C, Steele A, Downward J, Richeldi L, Lu X, Davies D, Jones M, Wang Y#. Autophagy inhibition-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in pulmonary fibrosis. Cell Death Dis 2019;10(8):591.
Liu H, Ertay A, Peng P, Li J, Liu D, Xiong H, Zou Y, Qiu H, Hancock D, Yuan X, Huang WC, Ewing RM, Downward J, Wang Y#. SGLT1 is required for the survival of triple negative breast cancer cells via potentiation of EGFR activity. Mol Oncol 2019;13(9):1874-1886.
Wang Y#, Xiong H, Liu D, Hill C, Ertay A, Li J, Zou Y, Miller P, White E, Downward J, Goldin RD, Yuan X and Xin Lu#. Autophagy inhibition specifically promotes epithelial-mesenchymal transition and invasion in RAS-mutated cancer cells. Autophagy 2019;15(5):886-899.
Yao L, Conforti F, Hill C, Bell J, Drawater L, Li J, Liu D, Xiong H, Alzetani A, Chee SJ, Marshall BG, Fletcher SV, Hancock D, Coldwell M, Yuan X, Ottensmeier CH, Downward J, Collins JE, Ewing RM, Richeldi L, Skipp P, Jones MG, Davies DE# and Wang Y#. Paracrine signalling during ZEB1-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in lung fibrosis. Cell Death Differ 2019;26(5):943-957.
Wang Y, Zhong S, Schofield CJ, Ratcliffe PJ, Lu X. Nuclear entry and export of FIH are mediated by HIF1α and exportin1, respectively. J Cell Sci 2018;131(22):jcs219782.
PhD Supervision
Charlotte Hill: Role of autophagy in the regulation of EMT, invasion and metastasis in RAS-mutated tumour. Funded by: Gerald Kerkut Charitable Trust and University’s Central VC Scholarship Scheme
Ayse Ertay: Functional analysis of SGLT1, a potential therapeutic target for PTEN-inactive breast cancer. Funded by: Wessex Medical Research
Liudi Yao: Epithelial-mesenchymal transition (EMT) induced by RAS activation in alveolar Type II cells leads to idiopathic pulmonary fibrosis (IPF) or lung cancer invasion? Funded by: China Scholarship Council Faculty / International Office Scholarship
Yilu Zhou: How does autophagy regulate the development of idiopathic pulmonary fibrosis (IPF)? Funded by: Institute for Life Sciences PhD Studentship/SoBS
Zijian Xu: Role of LKB1 in idiopathic pulmonary fibrosis (IPF) Funded by: China Scholarship Council Faculty / International Office Scholarship
Hualong Zhao: Effect of active ingredients from Limonium sinense extract on Epithelial-mesenchymal transition: implications in tumor invasion and lung fibrosis Funded by: International/SoBS
Idiopathic pulmonary fibrosis (IPF) is a life-threatening condition of the lungs where tissue becomes thickened, stiff, and scarred, limiting the amount of oxygen getting into the blood. The aim of this project is to provide effective targeted therapies for sufferers to reduce symptoms of this devastating disease and improve their quality of life as well as to identify biomarkers for IPF patients.
This project aims to identify molecular switches that can dictate the ability of RAS to contribute to either lung cancer or IPF using 3D culture and proteomics
This project aims to investigate the role of SGLT1 in the pathogenesis of PTEN-inactive breast cancer using cell biology, proteomics and biochemistry analysis.
FIH is an asparaginyl hydroxylase for HIFα and many ankyrin repeat domain (ARD) containing proteins.
The aim of this project is to understand how FIH regulates EMT and its implications in the development of IPF using integrated biochemical, transcriptomic, proteomic and imaging techniques.
Autophagy is a highly conserved and tightly regulated cellular process involved in the turnover of cytoplasmic organelles and proteins through a lysosome-dependent degradation process. The aim of this project is to understand the role of autophagy in the development of idiopathic pulmonary fibrosis (IPF), a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause.
School of Biological Sciences Invited Seminar Speaker Organiser
Dr Yihua Wang School of Biological Sciences Faculty of Environmental and Life Sciences Life Sciences Building 85 University of Southampton Highfield Campus Southampton SO17 1BJ
