Wan Hua

Research:

Currently I am working on the metabolic reprogramming during transforming growth factor (TGF)β-induced EMT of breast cancer cell lines. Metastasis is the leading cause of breast cancer related mortality. However, not all breast cancers have equal metastatic potential. One factor which contributes to metastatic potential is tumor invasiveness, which is promoted by the epithelial-mesenchymal transition (EMT). In the context of cancer, EMT is considered a fundamental step in the initiation of the metastatic cascade. The transcriptional and epigenetic reprogramming that governs EMT has been extensively characterized and reviewed in the last decade. However, increasing evidence demonstrates a correlation between metabolic reprogramming and EMT execution. Metabolism serves as a direct readout of cellular phenotype, and therefore the study of the altered metabolic pathways and metabolites associated with EMT will enhance our understanding of the global phenotypic changes underpinning this important physiological program. We are looking to analysis the metabolic reprogramming during TGFβ-induced EMT, and the metabolic effect of some pharmacological metabolomics compounds on EMT in breast cancer cells. Our aim is to define a metabolic signature associated with the EMT phenotype and assess its prognostic value for predicting patient outcome.

Curriculum Vitae:

My master work was performed at Sichuan University, Chengdu, China. My research was focus on component   characterization of phorbol esters from Jatropha curcas by using High-Speed Counter-Current Chromatography (HSCCC) and Ultra performance liquid chromatography (UPLC), in addition, we also evaluated the toxicity  of phorbol esters in mice model. My PhD study was concentrated  on the protective effects of Veronica ciliata Fisch. for ANIT-induced cholestatic liver injury and alcohol-induced liver injury in mice.