Introduction/Background Ovarian cancer (OC) is considered as the most lethal gynaecological disease, with epithelial ovarian cancer (EOC) being the most prevalent. The majority of OC patients are diagnosed at advanced stages and characterized by poor survival outcomes. Therefore, there is a critical need to identify effective screening tools for early detection. Long non-coding RNAs (lncRNAs) have emerged as significant regulators of gene expression. Bioinformatic analysis has revealed dysregulation of lncRNA RFX5-AS1 in a various cancers, including OC, indicating its potential as a biomarker. However, its functional role in OC is not well described.

Methodology In this study, we quantified RFX5-AS1 expression in a panel of OC cell lines using qRT-PCR. Silencing RFX5-AS1 and performed proliferation, invasion, and wound healing assays helped elucidate its functional role. To investigate its impact on chemoresistance modulation, A2780 S and A2780 CP cells were treated with malformin A1 (MA1), RFX5-AS1 levels were quantified. Additionally, qRT-PCR and western blotting were performed to assess the effect of RFX5-AS1 silencing on crucial cancer-related markers (YAP1, SOD2, BCL2).

Results RFX5-AS1 was found to be overexpressed in A2780CP and OVSAHO cells compared to the normal ovarian cell line (HOSE 6–3), leading to the silencing of RFX5-AS1 in these cell lines. However, knocking-down RFX5-AS1 did not impact proliferation, invasion, or wound healing. qRT-PCR and western blotting analysis revealed SOD2 downregulation in A2780 CP and lower levels of YAP1 and SOD2 in OVSAHO cells. Moreover, RFX5-AS1 was upregulated in MA1-treated A2780 CP cells compared to untreated cells. Pearson’s correlation analysis demonstrated a positive correlation between RFX5-AS1 and CDK4; RFX5 expression.

Conclusion This study highlights the regulatory effects of RFX5-AS1 silencing on ovarian carcinogenesis by targeting YAP1 and SOD2. Moreover, RFX5-AS1 shows potential in regulating MA1-induced cellular death in OC.

Disclosures The author’s declare no conflict of interest.