Alice Wang
Discovery of Cancer Cachexia Therapies Through a Novel Mouse Model
Abstract
The goal of this proposal is to elucidate the role of apelin in skeletal muscle during cancer cachexia (CC) development and recovery. I have developed a CC mouse model in which both CC development and recovery can be studied in the same animal. Using this model, I observed decreased muscle mass during CC development and increased muscle mass during CC recovery. By analyzing quadriceps RNA sequencing data from cachectic and recovering mouse, I identified increased denervation during CC development and increased reinnervation during CC recovery. This suggests that neuromuscular junctions (NMJ) may play a role in muscle atrophy and regeneration in CC. In addition, I identified apelin as the most upregulated hormone in the skeletal muscle during CC recovery. Apelin is anti-inflammatory and is involved in metabolism and muscle regeneration. My hypothesis is that apelin contributes to muscle atrophy and regain in CC development and recovery through NMJ disassembly and reassembly.
This fellowship will support my work on discovering novel therapies for patients with cancer cachexia and my career aspiration as a physician-scientist.
