biostudies-literatureHah YSNew Faculty Research Support Grant from Gyeongsang National University in 2025Biomedical Research Institute Fund from the Gyeongsang National University HospitalRegional Innovation System & Education (RISE) program through the RISE Center, Gyeongsang-nam-do, funded by the Ministry of Education (MOE) and the Gyeongsangnam-do Provincial Government, Republic of Korea522https://www.ebi.ac.uk/biostudies/studies/S-EPMC12896952biostudies-literatureUnknown18(3)Colorectal cancer (CRC) cachexia is a multifactorial, treatment-limiting syndrome characterized by progressive loss of skeletal muscle with or without loss of fat mass, accompanied by systemic inflammation, anorexia, metabolic dysregulation, and impaired treatment tolerance. Despite decades of work, cachexia remains clinically underdiagnosed and therapeutically underserved, in part because canonical models treat tumor-derived factors and host inflammatory mediators as a largely 'host-only' network. In parallel, CRC is strongly linked to intestinal dysbiosis, barrier disruption, and microbial translocation. Extracellular vesicles (EVs)-host small EVs, tumor-derived EVs, and bacterial extracellular vesicles (including outer membrane vesicles)-may provide a mechanistically plausible, informatCancersThe Vesicular Intersection Layer: A Framework for Cross-Kingdom Extracellular Vesicle Signaling That May Connect Gut Dysbiosis to Skeletal Muscle Wasting in Colorectal Cancer Cachexia.PMC128969522025-RISE-16-001GNU-NFRSG-0041GNUHBRIF-2025-0001Lee SJHah YSHwang JKwag SJfalseThe Vesicular Intersection Layer: A Framework for Cross-Kingdom Extracellular Vesicle Signaling That May Connect Gut Dysbiosis to Skeletal Muscle Wasting in Colorectal Cancer Cachexia.Colorectal cancer (CRC) cachexia is a multifactorial, treatment-limiting syndrome characterized by progressive loss of skeletal muscle with or without loss of fat mass, accompanied by systemic inflammation, anorexia, metabolic dysregulation, and impaired treatment tolerance. Despite decades of work, cachexia remains clinically underdiagnosed and therapeutically underserved, in part because canonical models treat tumor-derived factors and host inflammatory mediators as a largely 'host-only' network. In parallel, CRC is strongly linked to intestinal dysbiosis, barrier disruption, and microbial translocation. Extracellular vesicles (EVs)-host small EVs, tumor-derived EVs, and bacterial extracellular vesicles (including outer membrane vesicles)-may provide a mechanistically plausible, informat2026-01-01T00:00:00Z2026 Feb2026-07-07T03:12:59.598Z2026-07-07T03:08:32.86ZS-EPMC128969524168199510.3390/cancers18030522