RBPMS‐AS1 sponges miR‐19a‐3p to restrain cervical cancer cells via enhancing PLCL1‐mediated pyroptosis

Abstract Cervical cancer (CC) poses a threat to human health. Enhancing pyroptosis can prevent the proliferation and epithelial–mesenchymal transition (EMT) of tumor cells. This study aims to reveal the candidates that modulate pyroptosis in CC. Accordingly, the common microRNAs (miRNAs/miRs) that were sponged by RBPMS antisense RNA 1 (RBPMS‐AS1) and could target Phospholipase C–Like 1 (PLCL1) were intersected. The expression of PBPMS‐AS1/miR‐19a‐3p (candidate miRNA)/PLCL1 was predicted in cervical squamous cell carcinoma (CESC), by which the expression location of RBPMS‐AS1 and the binding between RBPMS‐AS1/PLCL1 and miR‐19a‐3p were analyzed. The targeting relationship between RBPMS‐AS1/PLCL1 and miR‐19a‐3p was confirmed by dual‐luciferase reporter assay. After the transfection, cell counting kit‐8 assay, colony formation assay, quantitative reverse transcription PCR, and Western blot were implemented for cell viability and proliferation analysis as well as gene and protein expression quantification analysis. Based on the results, RBPMS‐AS1 and PLCL1 were lowly expressed, yet miR‐19a‐3p was highly expressed in CESC. RBPMS‐AS1 overexpression diminished the proliferation and expressions of N‐cadherin, vimentin, and miR‐19a‐3p, yet enhanced those of E‐cadherin, PLCL1, and pyroptosis‐relevant proteins (inteleukin‐1β, caspase‐1, and gasdermin D N‐terminal). However, the above RBPMS‐AS1 overexpression–induced effects were counteracted in the presence of miR‐19a‐3p. There also existed a targeting relationship and negative interplay between PLCL1 and miR‐19a‐3p. In short, RBPMS‐AS1 sponges miR‐19a‐3p and represses the growth and EMT of CC cells via enhancing PLCL1‐mediated pyroptosis.