Role of long non-coding RNA-mRNA interactions in resveratrol-mediated inhibition of ovarian cancer cell proliferation.

Ovarian cancer (OC) is a prevalent gynecological malignancy requiring advancements in treatment. Resveratrol (RES), a natural polyphenolic compound, has attracted widespread attention due to its potent anticancer properties. Long non-coding (lnc)RNAs serve crucial regulatory roles in OC pathogenesis. However, the mechanism underlying the RES-mediated inhibition of OC cell proliferation through lncRNA regulation is not fully understood. The present study aimed to assess the role of lncRNAs in RES-mediated inhibition of OC cell growth. The A2780 OC cell line was used as the experimental model to establish control and RES-treated groups. The effect of RES on OC cell migration was also evaluated. Differentially expressed lncRNAs (DELs) were identified after RES treatment. lncRNA-mRNA regulatory networks of tumor-related pathways were constructed and functionally assessed using reverse transcription-quantitative PCR, proliferation assays, and knockdown and overexpression of hub lncRNAs. The results demonstrated that RES significantly inhibited OC cell migration. Moreover, 721 DELs were identified after RES treatment and were predominantly enriched in the p53 signaling pathway and cell cycle regulation associated with tumorigenesis. Key lncRNAs, including lnc-small nucleolar RNA host gene 15 (SNHG15)-203, demonstrated significant downregulation following RES treatment. Networks of tumor-associated mRNAs and their target lncRNAs also revealed an association with lnc-SNHG15-203. Furthermore, functional validation demonstrated that lnc-SNHG15-203 suppression markedly reduced the expression of the downstream targets H2A clustered histone (H2AC)7 and H2AC20, inhibiting cell proliferation. These results were consistent with the antiproliferative effects observed in RES-treated cells. Overall, the present study systematically characterized the lncRNA expression profiles associated with the RES-mediated inhibition of cell proliferation, establishing lnc-SNHG15-203 as a critical mediator of the anti-OC activity of RES. The findings could help to formulate strategies for improving OC treatment.