Background
Circular RNAs (circRNAs) are key players in tumorigenesis progression. However, the role and molecular mechanisms of circKCNQ5 in multiple myeloma (MM) progression remain unclear.
Conclusion
CircKCNQ5 was found to stimulate MM progression through competitively sponging to miR-335-5p.
Methods
The quantitative real-time polymerase chain reaction was used for examining circKCNQ5, miR-335-5p, and Bromodomain-containing protein 4 (BRD4) levels. The proliferation ability of MM cells was determined by Cell Counting Kit-8 and colony-forming assays. The migration and invasion were analyzed by transwell assay. Flow cytometry was used to assess cell apoptosis. The lactate production, glucose consumption, and ATP/ADP ratios were determined by commercialized kits. The protein levels were quantified by western blot analysis. The interactions between circKCNQ5 and miR-335-5p, along with miR-335-5p and BRD4 were analyzed by dual-luciferase reporter and RNA immunoprecipitation assays.
Results
The overexpression of circKCNQ5 was confirmed in MM tissues and cells. Importantly, knockdown of circKCNQ5 suppressed proliferation, migration, invasion, and glycolysis while it increased apoptosis of MM cells in vitro. Interestingly, the downregulation of miR-335-5p was able to rescue the circKCNQ5 inhibition-induced effects on MM cells. MiR-335-5p interacted with circKCNQ5, and was able to target BRD4 in MM cells. MiR-335-5p upregulation inhibited malignant phenotypes of MM cells depending on BRD4.