Hsa_circ_0006232 promotes laryngeal squamous cell cancer progression through FUS-mediated EZH2 stabilization
Tianyi Wu, Guangke Wang, Xianting Zeng, Zhanwei Sun, Shichao Li, Weiwei Wang, Boyu Yu
Abstract
Laryngeal squamous cell cancer (LSCC) is one of the most common malignant tumors in head and neck tumors. Our previous study has revealed that hsa_circ_0006232 is abnormally expressed in LSCC. This study attempts to verify the biological role of hsa_circ_0006232 in LSCC. We found that compared with human bronchial epithelial cells, hsa_circ_0006232 was highly expressed in human LSCC cells (AMC-HN-8 and TU686). Moreover, hsa_circ_0006232 promoted proliferation, migration and invasion of AMC-HN-8 and TU686 cells. Hsa_circ_0006232 promoted the expression of enhancer of zeste homolog 2 (EZH2) and repressed the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN). Fused in sarcoma (FUS) interacted with hsa_circ_0006232 and EZH2, and FUS promoted the stabilization of EZH2. Hsa_circ_0006232 inhibited PTEN by promoting FUS expression. Moreover, we constructed a tumor xenograft model by injection of AMC-HN-8 cells with hsa_circ_0006232 knockdown, and we found that hsa_circ_0006232 deficiency decreased tumor growth in mice. Hsa_circ_0006232 silencing repressed EZH2 expression and enhanced PTEN expression in tumor tissues. In conclusion, our data have demonstrated that Hsa_circ_0006232 promotes proliferation, migration and invasion of LSCC cells, and accelerates tumor growth of LSCC through FUS-mediated EZH2 stabilization. Thus, hsa_circ_0006232 may be a novel therapeutic target in LSCC treatment.