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It is known that the TGF-β superfamily receptors act as master regulators of cancer progression. However, alteration and role of type III TGF-β receptor (TβRIII, or betaglycan) as the most abundant of the TGF-β receptor has not been explored in salivary gland adenoid cystic carcinoma (ACC). Here, we reported that tumor biopsies and matched normal human salivary glands from patients with ACC were examined for the expression of TβRIII. The expression of TβRIII protein is significantly decreased in ACC patients based on immunohistochemistry and western blot analysis. In vitro, a transient overexpression of TβRIII markedly induced apoptosis and cell cycle arrest in the G2/M phase, thereby inhibited cell viability and migration of ACC-M cells. Co-immunoprecipitation revealed that TβRIII, scaffolding protein-arrestin2 (β-arrestin2) and IκBα formed a complex. Transient overexpression of TβRIII decreased p-p65 expression and increased IκBα expression, which was abolished by knockdown of β-arrestin2. The present study defines TβRIII as a biomarker exerting antitumor action on ACC progression.Gene therapy of TβRIII may be a powerful new approach for ACC disease.

Type III TGF-β receptor inhibits cell proliferation and migration in salivary glands adenoid cystic carcinoma by suppressing NF-κB signaling