Sorbs3, also known as vinexin, is an adaptor protein-encoding gene. It plays diverse roles in multiple biological processes. Sorbs3 is involved in regulating autophagy, cell-cell adhesion, and various signaling pathways such as YAP1-WWTR1/TAZ, Wnt/β-catenin, and IL-6/STAT3. It is crucial for normal development, like in dorsal root ganglion development, and is also associated with various diseases [1,2,3,4].

In brain aging, increased SORBS3 expression contributes to autophagic decline. SORBS3 depletion in cell lines, including mouse primary neurons, increases F-actin structures. These compete with YAP1-WWTR1/TAZ to bind AMOT proteins, allowing YAP1-WWTR1/TAZ to enter the nucleus and upregulate target genes, promoting autophagosome formation [1]. In cervical cancer, SORBS3-β, an isoform of SORBS3, suppresses lymph node metastasis. It binds to β-catenin, recruits UBA1 to enhance its ubiquitination and degradation, inhibiting Wnt/β-catenin signaling and downstream lymphangiogenesis pathways [2]. In lung adenocarcinoma, UBE2T mediates SORBS3 ubiquitination, enhancing IL-6/STAT3 signaling and promoting cancer progression [3].

In conclusion, Sorbs3 is a multi-functional gene involved in autophagy regulation, development, and cancer-related processes. Studies using cell lines and in vivo models, including those mimicking disease conditions, have revealed its role in brain aging, cervical cancer, and lung adenocarcinoma, providing potential therapeutic targets for these diseases.