Background: Emerging studies have indicated that circular RNAs (circRNAs) play important
roles in the development of many tumors. CircRNA-scavenger receptor class B member 1
(Circ-SCARB1) was consistently reported as an elevated circRNA in RCC tissues. This study focused
on examining the biological function and molecular mechanism of circSCARB1 in RCC progression.
Methods: Expressions of Circ-SCARB1, microRNA (miR)-510-5p, and syndecan 3 (SDC3) were
detected using a quantitative real-time polymerase chain reaction (RT-PCR) and/or western blot.
Cell proliferation and apoptosis were measured by 3-(4, 5)-dimethylthiahiazo (-z-y1)-3, 5-diphenytetrazoliumromide
and flow cytometry, respectively. Cell migration and invasion were measured
using Transwell assays. The interaction between miR-510-5p and Circ-SCARB1 or SDC3 was
verified using dual-luciferase reporter assays.
Results: Circ-SCARB1 was elevated in 30 pairs of RCC tissues and multiple RCC cell lines.
Knockdown of Circ-SCARB1 inhibited cell proliferation, migration, and invasion while inducing
cell apoptosis. MiR-510-5p was confirmed to be a target of Circ-SCARB1; inhibition of cell progression
by silencing Circ-SCARB1 was mediated by a direct interaction between Circ-SCARB1
and miR-510-5p. SDC3 was verified to be a gene target of miR-510-5p; transfection of miR-510-5p
mimic not only suppressed the expression of SDC3 but also the cell proliferation and an SDC3 cotransfection
partially restored cell proliferation. Additionally, the genetic knockdown of Circ-
SCARB1 reduced the expression SDC3, and the addition of anti-miR-510-5p could partially reelevate
Conclusion: Circ-SCARB1 promotes RCC progression via sequestering miR-510-5p and indirectly
up-regulating SDC3 expression. This provides a novel perspective for the pathogenesis of RCC and
potential therapeutic targets for the treatment of RCC.