Abstract
The action mechanism in which circular RNA (circ) SMARCA5 targeted nasopharyngeal carcinoma (NPC) cell proliferation, migration, invasion, and apoptosis via microRNA (miR)-582-3p/phosphatase and tensin homolog (PTEN) axis was explored. The examination was performed via reverse transcription-quantitative polymerase chain reaction (RT-qPCR), discovering that circSMARCA5 was elevated while miR-582-3p was silenced in NPC tissues and cells. E-cadherin and N-cadherin were detected. The results illustrated transfection with si-circSMARCA5 or miR-582-3p-mimic was available to repress cancer cell advancement, and E-cadherin was augmented. Transfection with pcDNA 3.1-circSMARCA5 or miR-582-3p-inhibitor was available to accelerate cancer cell advancement, and N-cadherin was augmented. MiR-582-3p-inhibitor blocked the suppression of si-circSMARCA5 on NPC. The si-PTEN blocked the malignant behavior of pcDNA 3.1-circSMARCA5 against NPC. The binding sites between circSMARCA5 and miR-582-3p and between miR-582-3p and PTEN were verified. Linear analysis results illuminated the expression pattern of circSMARCA5 was opposite to miR-582-3p, while the expression pattern of circSMARCA5 was positively associated with PTEN. In brief, the results of the research clarified circSMARCA5 modulated NPC cells' vital movement via the miR-582-3p/PTEN molecular axis.