Propranolol exhibits activity against hemangiomas independent of beta blockade

Propranolol is a widely used beta blocker that consists of a racemic mixture of R and S stereoisomers. Only the S stereoisomer has significant activity against the beta-adrenergic receptor. A fortuitous clinical observation was made in an infant who received propranolol for cardiac disease, and regression of a hemangioma of infancy was noted. order to gain further insights in the mechanisms of action of R-propranolol in vivo, we subjected vehicle- and R-propranolol-treated tumors to RNAseq analysis. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that choline metabolism was the pathway most affected by R-propranolol treatment. Consistent with this, the most highly regulated gene by R-propranolol treatment was Betaine-Homocysteine Methyl Transferase (Bhmt). Other genes that are involved in tumor suppressive activities such as Early Growth Response 1 (Egr1) and AP-1 subunit, which are both transcription factors implicated in tumor suppression. Egr1 regulates important tumor suppressors such as PTEN and p53, and upregulates tumor necrosis factor α (TNF-α). Fos, which has been known to be rearranged and expressed frequently in epithelioid hemangioma, was also upregulated in R-propranolol-treated samples. The genes identified in the RNAseq analysis pose as interesting targets for further investigations. Analysis of transcriptome regulation in R-propranolol treated tumors