Secretariat, Alumni Association, IDAC
Date	Tuesday, 30 September 2025, 16:00～
Room	7th Floor, Seminar Room 1, IDAC Center for Basic Aging Research
Title	Tumor–Muscle Crosstalk: Insights into Cachexia-Associated miRNAs
Speaker	Dr. Hong-Wen Tang
Affiliation	Program in Cancer and Stem Cell Biology, Duke-NUS Medical School
Organizer	Shinpei Kawaoka (Dept. Integrative Bioanalytics, ext.8568)
Abstract	Cancer cachexia, a debilitating syndrome characterized by progressive skeletal muscle loss, significantly worsens cancer patient outcomes. Despite its impact, the mechanisms underlying cancer cachexia remain poorly understood, and effective therapies are unavailable. Muscle stem cells (MuSCs) are critical for muscle repair, making the regulation of muscle regeneration a promising therapeutic target. However, the molecular pathways impairing MuSC function in cachexia are largely unexplored. Through in vivo Drosophila screens, we identified LC3-dependent extracellular vesicles (LC3 EVs) as mediators of tumor-induced muscle wasting. Depletion of LC3 EVs alleviated muscle wasting in tumor-bearing flies. Translational studies in mice confirmed that LC3 EVs suppress muscle regeneration, and microRNA sequencing revealed that miR-30a-3p, carried by LC3 EVs, negatively regulates muscle regeneration by targeting Myocyte Enhancer Factor 2C. Inhibiting miR-30a-3p with antagomirs restored muscle regeneration and rescued muscle wasting in cachectic mice. Clinical data showed that plasma LC3 EV and miR-30a-3p levels strongly correlate with cachexia severity in cancer patients, highlighting their potential as biomarkers and therapeutic targets. This study uncovers a novel tumor-muscle interaction mediated by LC3 EVs and miR-30a-3p, providing new insights into cancer cachexia pathogenesis and a basis for innovative diagnostic and therapeutic approaches.