ABSTRACT
OBJECTIVES: The aim of our study was to explore the role of circular RNA_0061140 (circ_0061140) in adenomyosis progression and its associated mechanism. DESIGN: We first analyzed the expression pattern of circ_0061140 in endometrial tissues of adenomyosis patients (n = 27) and uterine fibroid patients (n = 15). Loss-of-function experiments were conducted to analyze the biological roles of circ_0061140 in regulating the viability, apoptosis, proliferation, migration, and invasion of endometrial epithelial cells. The downstream microRNA (miRNA)/messenger RNA (mRNA) axis of circ_0061140 was predicted by bioinformatics tool Starbase, and its working mechanism was verified by rescue experiments. METHODS: Cell viability, apoptosis, proliferation, invasion, and migration were assessed by cell counting kit-8 assay, flow cytometry analysis, 5-ethynyl-2'-deoxyuridine assay, transwell assay, and scratch test. The binding relationship between miR-141-3p and circ_0061140 or lin-28 homolog B (LIN28B) was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. RESULTS: Circ_0061140 expression was upregulated in adenomyosis patients. Circ_0061140 knockdown suppressed the viability, proliferation, invasion, and migration and triggered the apoptosis of endometrial epithelial cells. Circ_0061140 served as a miRNA sponge for miR-141-3p, and miR-141-3p silencing partly reversed circ_0061140 knockdown-induced effects in endometrial epithelial cells. miR-141-3p directly interacted with LIN28B mRNA. LIN28B overexpression partly diminished miR-141-3p overexpression-mediated influences in endometrial epithelial cells. Circ_0061140 knockdown downregulated LIN28B expression by elevating miR-141-3p level in endometrial epithelial cells. LIMITATIONS: The functional verification of circ_0061140/miR-141-3p/LIN28B axis was merely conducted in vitro. CONCLUSION: Circ_0061140 contributed to adenomyosis progression by binding to miR-141-3p to induce LIN28B expression in vitro.
