Abstract
CircularRNAs(circRNAs)havebeenconfirmedtobeanimportantmodulatorandtherapeutictargetofcervicalcancer(CC).Theaimofthisstudyistoexploretheroleandmechanismofcirc_0081723inCCprogression. Circ_0081723,microRNA-545-3p(miR-545-3p), and CREB3regulatoryfactor(CREBRF) levels were detected using quantitativereal-timePCR (qRT-PCR) assay. CREBRF, ki-67,Bcl-2 related X protein (Bax), andE-cadherinexpression levels were determined using western blot (WB) and immunohistochemistry (IHC) assays. Cell proliferation was assessed using Cell Counting Kit-8 (CCK-8), cell colony formation, and 5-ethynyl-2'-deoxyuridine (EdU) assays. Flowcytometry was used to measurecellapoptosis. Cell migration and invasion were examined using Transwellassay. Interaction between miR-545-3p and circ_0081723 or CREBRF was verified using dual-luciferasereporterassay and RNAimmunoprecipitation (RIP) assays. The biological role of circ_0081723 on CC growth was examined using the xenograft tumor model in vivo. Circ_0081723 and CREBRF were increased, and miR-545-3p was decreased in CC tissues and cells. Circ_0081723 silencing suppressedCCcellgrowthandmotilitywhereasboostedCCcellapoptosis.Besides,circ_0081723actedasamolecularspongeformiR-545-3p,andcirc_0081723knockdown-inducedeffectswerelargelyreversedbymiR-545-3pdownregulationinCCcells.Moreover,miR-545-3prepressedCCprogressionbytargetingCREBRF.Circ_0081723absenceblockedxenografttumorgrowthinvivo. Circ_0081723stimulatedCCcellmalignantbehaviorsbyregulatingthe miR-545-3p/CREBRFpathway,providingapossiblecircRNA-targetedtherapyforCC.
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