Caveolin-1 Mediates Low-Intensity Ultrasound-Induced Apoptosis via Downregulation of Signal Transducer and Activator of Transcription 3 Phosphorylation in Laryngeal Carcinoma Cells

Abstract

Low-intensity ultrasound therapy has been found to be a potential tool in the management of malignant tumors in recent years. However, the molecular mechanism underlying low-intensity ultrasound-induced apoptosis is still not clear. In this study, we investigated the effects of low-intensity ultrasound-induced apoptosis in HEp-2 cells. We found that low-intensity ultrasound significantly induced apoptosis, and the expression level of caveolin-1 (Cav-1) was dramatically increased after ultrasound treatment of HEp-2 cells. After inhibiting the expression level of Cav-1 using siRNA transfection, we found that the cellular apoptosis induced by low-intensity ultrasound was significantly suppressed. In addition, inhibition of Cav-1 expression promoted phosphorylation of signal transducer and activator of transcription 3 (STAT3), suggesting that the STAT3 signaling pathway was involved in low-intensity ultrasound-induced apoptosis via Cav-1 regulation. Our results indicate that Cav-1/STAT3 signaling pathway may mediate low-intensity ultrasound-induced apoptosis, and this technology could potentially be used clinically for the treatment of cancers.

Keywords: Apoptosis; Caveolin-1; Low-intensity ultrasound; STAT3.