Abstract：Objective: To investigate the role of circZNF609 in angiogenesis of ovarian cancer cells and its potential mechanism. Methods: The OVCAR3 cells were divided into 10 groups with three replicate wells each: si-NC group (transfected with control si-NC), si-ZNF609 group (transfected with si-ZNF609), NC mimic group (transfected with NC mimic), miR-150-5p mimic group (transfected with miR-150-5p mimic), NC inhibitor group (transfected with NC inhibitor), miR-150-5p inhibitor group (transfected with miR-150-5p inhibitor), si-ZNF609 + NC inhibitor group (cotransfected with si-ZNF609 and NC inhibitor), si-ZNF609 + miR-150-5p inhibitor group (cotransfected with si-ZNF609 and miR-150-5p inhibitor), si-ZNF609 + pcDNA-NC group (cotransfected with si-ZNF609 and pcDNA-NC), and si-ZNF609 + pcDNA-VEGF group (cotransfected with si-ZNF609 and pcDNA-VEGF). RT-qPCR was used to detect the expression levels of ZNF609 and miR-150-5p, while Western blot was employed to measure the expression level of VEGF. Plate cloning and Transwell assays were conducted to assess the proliferation activity and invasion ability of OVCAR3 cells. An in vitro Matrigel tube formation assay was performed to evaluate angiogenesis. Results: Compared with the normal human ovarian epithelial cell line IOSE80, the expression of ZNF609 was significantly increased, while the expression of miR-150-5p was significantly decreased in human ovarian cancer cell lines (P<0.05). Compared with the si-NC group, the si-ZNF609 group exhibited significantly reduced expression of ZNF609 and VEGF, cell clone numbers, transmembrane cell counts, and the number of formed tubules, along with a significant increase in miR-150-5p expression (P<0.05). In comparison with the si-ZNF609 + NC inhibitor group, the si-ZNF609 + miR-150-5p inhibitor group showed significantly increased cell clone numbers, transmembrane cell counts, and formed tubule numbers, as well as a significant decrease in miR-150-5p expression (P<0.05). The miR-150-5p mimic group had significantly lower VEGF expression levels compared with the NC mimic group (P<0.05), whereas the miR-150-5p inhibitor group showed significantly higher VEGF expression levels compared with the NC inhibitor group (P<0.05). When compared with the si-ZNF609 + pcDNA-NC group, the si-ZNF609 + pcDNA-VEGF group exhibited significantly increased VEGF expression levels, cell clone numbers, transmembrane cell counts, and formed tubule numbers (P<0.05). Conclusion: circZNF609 is highly expressed in ovarian cancer, and knockdown of its expression can inhibit angiogenesis in ovarian cancer cells. This mechanism may be related to the regulation of miR-150-5p/VEGF axis by circZNF609.
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2025, Vol. 31 
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