Circular RNA hsa{sub c}irc{sub 0}000673 promotes hepatocellular carcinoma malignance by decreasing miR-767-3p targeting SET
Highlights: • Hsa{sub c}irc{sub 0}000673 was highly expressed in HCC tissues. • Hsa{sub c}irc{sub 0}000673 knockdown suppressed HCC cell proliferation and invasion. • Hsa{sub c}irc{sub 0}000673 promoted HCC proliferation and invasion by sponging miR-767-3p. • Hsa{sub c}irc{sub 0}000673 facilitated HCC cell proliferation and invasion via regulating miR-767-3p/SET pathway. The importance of circular RNAs (circRNAs) in human cancers has gradually been acknowledged. In hepatocellular carcinoma (HCC), several circRNAs have been reported to regulate tumor growth and metastasis. However, the role of hsa{sub c}irc{sub 0}000673 in HCC remains largely unknown. In this study, we found that hsa{sub c}irc{sub 0}000673 was significantly upregulated in HCC tissues compared to adjacent non-tumor tissues. Moreover, we found that hsa{sub c}irc{sub 0}000673 knockdown markedly inhibited the proliferation and invasion of HCC cells in vitro. Besides, hsa{sub c}irc{sub 0}000673 silence led to delayed tumor growth in vivo. In terms of mechanism, we showed that hsa{sub c}irc{sub 0}000673 directly associated with miR-767-3p in HCC cells. Via inhibiting miR-767-3p, hsa{sub c}irc{sub 0}000673 promoted HCC cell proliferation and invasion. Furthermore, we demonstrated that SET was a downstream effector of hsa{sub c}irc{sub 0}000673/miR-767-3p signaling. We showed that miR-767-3p could significantly promote SET expression by sponging miR-767-3p in HCC cells. Finally, rescue assays indicated that SET expression was essential for the effects of hsa{sub c}irc{sub 0}000673/miR-767-3p signaling on HCC cell proliferation and invasion. Taken together, our findings demonstrated that hsa{sub c}irc{sub 0}000673 promoted HCC malignant behaviors via regulating miR-767-3p/SET pathway.