School of Biomedical Sciences cordially invites you to join the following seminar:

Speaker: Professor Kweon Yu, Professor, Metabolism and Neurophysiology Research Group, Korea Research Institute of Bioscience & Biotechnology & Department of Functional Genomics, University of Science and Technology, South Korea
Talk Title: Feeding regulation in cancer-associated anorexia

Date: 1 November 2024 (Friday)
Time: 5:00 pm – 6:00 pm
Venue: Seminar Room 4, G/F, Laboratory Block, 21 Sassoon Road
Host: Professor Jung Kim

Biography

Prof. Kweon Yu is a Molecular Geneticist, studying neuropeptide signaling and feeding regulation, and Tau degradation using the Drosophila model system. He received his Ph.D. in Developmental Genetics from Bowling Green State University, Ohio, USA in 1994. Then, he had postdoctoral training at the University of California, San Diego from 1994-1999. He studied neural development with Dr. Ethan Bier at the Department of Biology. In 1999, he started his lab at the Shriners Hospital for Children, California, where he studied neuropeptide signaling. At the end of 2001, he moved to the Korea Research Institute of Bioscience & Biotechnology (KRIBB) and continued the research on neuropeptide signaling and feeding regulation. Recently, his research interest was expanded to Tau degradation in Alzheimer’s disease, and he performed collaborative research with the Dementia Research Center at the Korea Institute of Science and Technology (KIST), South Korea.

Abstract

In advanced-stage cancer patients, cancer-associated anorexia affects treatment success and patient survival; however, the underlying mechanism is poorly understood. I present that Dilp8, a Drosophila homolog of mammalian INSL3, is secreted from tumor tissues and induces anorexia through the Lgr3 receptor in the brain. Activated Dilp8-Lgr3 signaling upregulated anorexigenic nucleobinding 1 (NUCB1) and downregulated orexigenic short neuropeptide F (sNPF) and NPF expression in the brain. In the cancer condition, the protein expression of Lgr3 and NUCB1 was significantly upregulated in neurons expressing sNPF and NPF. Insulin-like 3 (INSL3) levels were increased in tumor-implanted mice and INSL3-treated mouse hypothalamic cells showed Nucb2 upregulation and Npy downregulation. Food consumption was significantly reduced in intracerebrospinal INSL3-injected mice. In human pancreatic cancer patients, higher serum INSL3 levels increase anorexia. These results indicate that tumor-derived Dilp8/INSL3 induces cancer anorexia by regulating feeding hormones through the Lgr3/Lgr8 receptor in Drosophila and mammals.

ALL ARE WELCOME.