Treatment options for advanced metastatic or progressive thyroid cancers are 
limited. Although targeted therapy specifically inhibiting intracellular kinase 
signaling pathways has markedly changed the therapeutic landscape, side-effects 
and resistance of single agent targeted therapy often leads to termination of 
the treatment. The objective of the present study was to identify the antitumor 
property of the non-selective β-adrenergic receptor antagonist propranolol for 
thyroid cancers. Human thyroid cancer cell lines 8505C, K1, BCPAP and BHP27 were 
used in the present study. Broad β-blocker propranolol and β2-specific 
antagonist ICI118551, but not β1-specific antagonist atenolol, inhibited the 
growth of 8505C and K1 cells. Propranolol treatment inhibited growth and induced 
apoptosis of 8505C cells in vitro and in vivo, which are closely associated with 
decreased expressions of cyclin D1 and anti-apoptotic Bcl-2. Expression of 
hexokinase 2 (HK2) and glucose transporter 1 (GLUT1) also decreased following 
propranolol intervention. 18F-FDG PET/CT imaging of the 8505C xenografts 
validated shrinkage of the tumors in the propranolol-treated group when compared 
to the phosphate‑buffered saline treated group. Finally, we found that 
propranolol can amplify the cytotoxicity of vemurafenib and sensitize thyroid 
cancer cells to cytotoxic effect of vemurafenib. Our present results suggest 
that propranolol has potential activity against thyroid cancers and 
investigation of the combination with targeted molecular therapy for progressive 
thyroid cancers could be beneficial.