Dr Xiao-Ming Sun

Biography:

Xiao-Ming trained as a Pharmacist in the Nanjing College of Pharmacy, Nanjing, China. After a few years working in the China Pharmaceutical Incorporation, he took a 3-year research degree course (MSc) in Pharmacology at the China Pharmaceutical University and worked on the effect of components of a Chinese traditional herb on the metabolism of arachidonic acid and platelet aggregation. After a few years teaching and research in Pharmacology and Toxicology, he gained a 1-year grant from the British Council to train in Toxicology at the MRC Toxicology Unit (Carshalton, Surrey) with Dr. Gerry Cohen followed by a PhD program in Biochemistry studying the nuclear morphological changes and related biochemical events that occur during apoptosis. Following a brief Postdoctoral Fellowship with Prof. David Ross at Colorado University, USA studying the effect of metabolically activated compounds (either environmental toxins or purposely designed drugs) on cellular toxicity/induction of apoptosis, Xiao-Ming rejoined Prof. Gerry Cohen’s group to study the molecular mechanisms of apoptosis. Following Prof. Cohen’s retirement in 2012, Xiao-Ming joined the lab of Prof. Marion MacFarlane where he continues to study the fundamental mechanisms of cell death. He has also applied his extensive experience to the Cross-Unit project exploring fibre-induced toxicity (including mesothelioma), with a focus on understanding mechanisms of apoptosis resistance as an adverse outcome following pathogenic fibre exposure.

Research Interests:

Cell death is vital for the survival of multicellular organisms, not only during development, to shape the morphogenesis of tissues and organs, but also in the maintenance of homeostasis in adults. Apoptosis is a mode of cell death defined by a characteristic morphology with distinct cell biological and biochemical features. In toxicology, abnormally induced apoptosis is an indication of the toxicity caused by environmental substances or medicinal products. My research interests focus on the activation mechanism of caspases, key executioners of the apoptotic death program, and their functional analysis. Currently, I am studying the mitochondria-mediated intrinsic cell death pathway with a specific emphasis on the interaction of BCL-2 family members and their role in formation of mitochondrial outer membrane permeability (MOMP) leading to the activation of caspases. For this, we combine our knowledge of the metabolic reprogramming of tumour cells with the regulation of BCL-2 family members to sensitise mesothelioma cells (a clinically incurable cancer related to the inhalation of asbestos or other hazardous fibres) to newly developed, purpose-designed drugs that target the Bcl-2 family. Meanwhile, I am also interested in demonstrating the mechanisms of cardiotoxicity induced by this class of newly designed drugs.