Current position:

Associate Professor

Department of Biochemistry & Molecular Biology and Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taiwan, Republic of China

Liver Research Center, Chang Gung Memorial Hospital, LinKuo, Taiwan, Republic of China

Relevant experience:

Assistant Professor in Department of Biochemistry & Molecular Biology and Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taiwan, Republic of China (2012/2~2022/8)

Postdoctoral Research Fellow in Institute of Biomedical Sciences, Academia Sinica (2007/3~ 2012/2)

Postdoctoral Research Fellow in Graduate Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University (2005/7~2005/11)

Contact information:

Tumor Research Laboratory

The 6th Floor, 1st Medicine Building

No. 259 Wen-Hwa 1st Road, Kwei-Shan Tao-Yuan,Taiwan33302, R.O.C

Tel: +886-3-2118800 ext 5115

  Autophagy is a stress-responsive process (such as nutrient starvation) that catabolizes cytoplasmic components to maintain the cellular homeostasis. Autophagy initiates with the rearrangement of membranous structures and coordinates with the cascades of signal transduction. Then, the cytoplasmic components are initially sequestered by a membrane-constituted structure, named isolation membrane (IM) or phagophore, which then expands and the two ends meet to form a double-membraned vesicle termed autophagosome. Finally, autophagosome fuses with a lysosome, forming the autolysosome where the engulfed cytoplasmic contents are degraded. The autophagic machinery has long been known to act as a stress response that promotes cell survival, mainly by regulating the energy availability and maintaining the organelle quality. Nevertheless, emerging evidence indicates that autophagy may function in regulating multiple defensive responses to microbial infections, such as degrading the invading microorganisms including bacteria, viruses, and protozoa, activating the host immune response against these infecting pathogens, or suppressing host innate immunity to help replication of the invading virus. On the other hand, autophagy is also activated by virus infection to promote the viral life cycle. Therefore, study on how autophagy is regulated is important will promote our understanding of how cell counteracts stresses. In the future, we set up three goals as the follows,

1. Several viral infections have shown to activate autophagy. Our recent study demonstrates that HCV induces autophagic process via unfolded protein response (UPR) (Journal of Clinical Investigation). Our results reveal that HCV-induced autophagy suppresses innate antiviral immunity to promote viral RNA replication in the infected cells. However, how autophagy promotes HCV escape from immune surveillance is largely unknown. To answer this question, we will employ molecular biology, proteomics, and transmission electron microscopy to investigatehow autophagy represses antiviral immunity by altering signal transduction and protein trafficking of innate immunity-associated molecules. 

2. Virus infection often activates autophagy via UPR. Current studies indicate that virus replication within the endoplasmic reticulum-associated membranous structure may trigger stress response to induce UPR, thus activate autophagy. However, the detailed molecular mechanism underlying how UPR promotes autophagy is thus far poorly understood. In the future, we will utilize the siRNA interference technology and transcriptional genomics to investigate the functional role of UPR in the activation of autophagic process. The regulation of gene transcription, protein synthesis, and post-translational modifications of proteins involved in this process will be analyzed.

3. Autophagy plays a promoting and/or repressive role in tumorigenesis. So far, the related studies regarding the function of autophagy in the progress of tumor formation is still controversial. In the future, our study will focus on investigation of the physiological significance of autophagy in the pathogenesis of liver cancer.