〔Abstract〕 Objective To explore the role of long non-coding RNA PITPNA-AS1 in ovarian cancer and its possible molecular mechanism. Methods Fluorescence real-time quantitative polymerase chain reaction(qPCR) technology was used to detect the expression level of PITPNA-AS1 in ovarian cancer tissues and corresponding adjacent tissues, ovarian cancer cell lines and normal ovarian epithelial cell lines. The cell lines with the least expression of PITPNA-AS1 were divided into control group and experimental group, and transfected with negative control plasmid or PITPNA-AS1 plasmid respectively. Cell counting(CCK-8) method and Transwell method were used to detect cell proliferation activity and invasion ability. Bioinformatics methods and dual luciferase activity reporter gene experiments predicted and verified the molecular mechanism of PITPNA-AS1. qPCR and Western blot were used to detect the gene expression of PITPNA-AS1 interaction. Results The expression of PITPNA-AS1 in ovarian cancer tissues was lower than that in adjacent tissues(P<0.01). The expression level of PITPNA-AS1 in ovarian cancer cell lines was lower than that in normal ovarian epithelial cells(P<0.05), and the expression in OVCAR-3 cells was the least(P<0.01). Compared with the control group, overexpression of PITPNA-AS1 could inhibit the proliferation activity(P<0.05) and invasion ability(P<0.01) of OVCAR-3 cells. PITPNA-AS1 had a targeting relationship with miR-92 a-3 p(P<0.01), and miR-92 a-3 p had a targeting relationship with transcription factor 21(TCF21)(P<0.01). Overexpression of PITPNA-AS1 caused a decrease in the expression of miR-92 a-3 p in OVCAR-3 cells(P<0.01), and an increase in the expression of TCF21 gene(P<0.01). Conclusion PITPNA-AS1 is lowly expressed in ovarian cancer tissues and cell lines. PITPNA-AS1 can inhibit the proliferation and invasion of ovarian cancer OVCAR-3 cells through targeted regulation of miR-92 a-3 p/TCF21.