Circular RNAs (circRNAs) play vital regulatory roles in the development of ovarian cancer (OC). However, the functions of circRNA Atlastin GTPase 2 (circATL2) in paclitaxel (PTX) resistance of OC are still unclear. As a result, circATL2 was upregulated in PTX‐resistant OC tissues and cells. CircATL2 knockdown reduced IC50 of PTX, inhibited colony formation ability and promoted cell cycle arrest and apoptosis in PTX‐resistant OC cells. Silencing of circATL2 restrained PTX resistance in vivo. Furthermore, miR‐506‐3p could be targeted by circATL2 and miR‐506‐3p inhibition reversed the impacts of circATL2 knockdown on PTX resistance and cell progression in PTX‐resistant OC cells. NFIB was identified as the target of miR‐506‐3p. MiR‐506‐3p overexpression suppressed PTX resistance and malignant behaviors of PTX‐resistant OC cells, with NFIB elevation rescued the impacts. To summarize, circATL2 promoted the resistance of OC to PTX by sponging miR‐506‐3p to upregulate NFIB expression, providing a new sight in chemoresistance of OC.

No abstract