吳珊瑩 Shan-Ying Wu

Innovative Insights into Secretory Autophagy and Disease

My research primarily focuses on autophagy and its roles in cellular processes. Early in my career, I investigated degradative autophagy in liver cancer progression. I was the first to demonstrate that the oncogene CCND1 was degraded through the autophagic pathway. Beyond elucidating the regulatory mechanisms between oncogenic factors and autophagy, I analyzed liver cancer patient samples to bridge basic research and clinical applications and validated the tumor-suppressive effects of autophagy in animal models. Notably, my team was the first to report that miRNA was encapsulated in autophagosomes, leading us to explore how the autophagic pathway regulates miRNA homeostasis in different cancers. These studies expanded our understanding of autophagy and offered new perspectives for cancer research.

As my research evolved, I recognized the significance of secretory autophagy as an emerging field. I began exploring the regulation mechanisms of secretory autophagy in physiology and pathology. We are the first to demonstrate that secretory autophagy facilitates viral release using a dengue virus-infected lung cell model and a novel autophagosome purification technique. Additionally, we identified vesicle transport-related proteins, such as RAB and SNARE, in secretory autophagosomes, which opened new research directions. By studying insulin secretion (physiology) and lung cancer metastasis (pathology), we confirmed the key role of RAB37 in secretory autophagy.

Beyond my lab, I actively collaborate with other teams to investigate the regulation of autophagy in various physiological and pathological contexts. These collaborations have yielded significant insights into my future research. I will focus on secretory autophagy, particularly its role in viral infections and immune microenvironment modulation. I aim to uncover novel mechanisms, integrate findings with clinical applications, and ultimately contribute to innovative therapeutic strategies.