Tgfbr3, also known as betaglycan, is a co-receptor in the TGF-β signaling pathway. The TGF-β superfamily signaling pathways are involved in multiple biological processes such as embryonic development, cellular homeostasis regulation, and immune function [1,2,3,4,5,6].

In various cancer types, Tgfbr3 shows distinct roles. In lung cancer, its expression decreases, and this reduction is closely related to the invasion, metastasis, angiogenesis, and apoptosis of lung cancer cells, acting as a tumor suppressor [1]. In breast cancer, Tgfbr3 mediates anoikis by suppressing ATF4 signaling, and its loss is associated with cancer progression [2]. In papillary thyroid cancer, Tgfbr3 inhibits tumor progression by inhibiting the PI3K/AKT pathway and epithelial-mesenchymal transformation (EMT), with low expression correlating with poor prognosis [3]. In contrast, in esophageal squamous cell carcinoma, Tgfbr3 is overexpressed, and high expression is associated with poor prognosis, making it a potential prognostic marker and therapeutic target [4]. In thyroid-eye disease, the miR-103a-3p/Tgfbr3 axis regulates TGF-β-induced orbital fibroblast activation and fibrosis [5]. In myocardial infarction, the let-7-Tgfbr3-p38 MAPK signaling is involved in cardiomyocyte apoptosis, and Tgfbr3 may serve as a biomarker and therapeutic target [6].

In conclusion, Tgfbr3 is a crucial component of the TGF-β signaling pathway, playing diverse roles in different biological processes and disease conditions, especially in various cancers, myocardial infarction, and thyroid-eye disease. Understanding its functions through studies in different disease models provides insights into disease mechanisms and potential therapeutic strategies.