Che WeiChang Institute of Basic Medical Sciences, National Cheng Kung UniversityTaiwan

I am currently a postdoctoral researcher at the Institute of Basic Medical Sciences, National Cheng Kung University. My research focuses on two major areas: metabolic regulation in pancreatic islet cells in metabolic diseases, and the role of epigenetics in tumor–host interactions. During my Ph.D. training, I identified that the heterochromatin protein HP1a (homologous to HP1α in mammals) plays a critical tumor-suppressive role under metabolic stress. Furthermore, I identified and characterized its downstream target, the gluconeogenic gene PEPCK1, which is aberrantly upregulated in high-sugar diet–induced tumors. Suppression of PEPCK1 significantly attenuated tumor progression, revealing a novel “epigenetic–metabolic” regulatory axis. Following completion of my military service, I am now in the first year of my postdoctoral training, where my research has expanded in two directions. First, I continue to utilize the Drosophila model to investigate the protective role of HP1a in cancer cachexia and to further dissect the mechanisms of inter-organ communication between tumors and the host. Second, I employ mouse models combined with single-cell transcriptomic analysis to study the physiological function of the phosphatase DUSP2 in the pancreas, with a particular focus on its role in β-cell plasticity and transdifferentiation. Overall, my research aims to elucidate how HP1-mediated heterochromatin contributes to tumor progression and regulates cancer cachexia in the host, while identifying potential therapeutic targets to advance translational cancer research. Now I am actively investigating the role of DUSP2, integrating both mouse and Drosophila models to explore its function in pancreatic biology, metabolic diseases, and pancreatic cancer, particularly in the context of β-cell plasticity and transdifferentiation.