Background: While emerging evidence indicates that circHIPK3 is critically involved in tumorigenesis and the development of several cancers, its role in prostate cancer (PCa) is not clearly understood.
Materials and methods: Human PCa samples and their matched normal adjacent tissues were obtained from 26 patients to assess the expression of circHIPK3 and its relationship with PCa prognosis. A series of in vitro and in vivo functional experiments were carried out to elucidate the role of circHIPK3 in PCa progression and its underlying molecular mechanisms.
Results: In this study, we found that circHIPK3 was overexpressed in PCa tissues and that higher circHIPK3 expression was associated with tumor stage. Moreover, circHIPK3 knockdown markedly inhibited the proliferation, migration, and invasion of PCa cells in vitro and impaired tumor growth in vivo. Bioinformatics analysis and luciferase reporter assays demonstrated that circHIPK3 could promote MCL1 expression by interacting with miR-193a-3p in PCa. Finally, rescue assays illustrated that circHIPK3 knockdown could partially reverse the effects of MCL1 overexpression.
Conclusion: In summary, our study illustrated, for the first time, that circHIPK3-mediated miR-193a-3p-MCL1 signaling promotes PCa development and progression, providing a novel therapeutic target for PCa.
Keywords: MCL1; circHIPK3; circular RNA; miR-193a-3p; prostate cancer.