Avil, also known as advillin, is a novel oncogenic actin-binding protein. It plays a role in many cytoskeletal functions and may function upstream of two oncogenic pathways, PAX3-FOXO1 and RAS, thus being of great biological importance in related cellular processes [1,2].

In rhabdomyosarcoma (RMS), AVIL is overexpressed in many RMS cell lines, patient-derived xenograft models, and clinical samples of both alveolar (ARMS) and embryonal (ERMS) subtypes. Silencing AVIL in RMS cells with its overexpression nearly eradicated the cells in culture and inhibited in vivo xenograft growth in mice. Conversely, gain-of-function manipulations of AVIL led to increased cell growth and migration, and transformed mesenchymal stem cells in vitro and in vivo. This indicates AVIL is a critical factor in RMS tumorigenesis and maintenance [1,2].

In conclusion, Avil is an important actin-binding protein with a key role in cytoskeletal functions. Its dysregulation is closely associated with RMS, and studies on Avil, especially through loss-of-function experiments in models like in vivo mouse xenografts, have revealed its significance in this pediatric soft-tissue cancer, providing potential directions for targeted therapies [1,2].