BCL2L1 is identified as a target of naringenin in regulating ovarian cancer progression.

Naringenin is a natural bioactive flavonoid with a wide spectrum of biological activities, including anti-carcinogenic ability. Our study aimed to investigate the effect of naringenin on ovarian cancer (OC) progression. Naringenin was input into PharmMapper and SwissTargetPrediction databases to predict its targets, and OC-related targets were obtained using MalaCards and GEPIA databases, which were imported into online Venn tool to identify the common targets. B-cell lymphoma-2 like 1 (BCL2L1) expression in OC tissues and cells was detected using GEPIA and HPA databases, qRT-PCR and Western blot analysis. The prognostic and diagnostic values of BCL2L1 in OC were determined using Kaplan-Meier plotter tool and receiver operating characteristic (ROC) curve analysis, respectively. Cell proliferation was evaluated using CCK-8 and EdU incorporation assays. Cell apoptosis was determined using TUNEL and caspase-3 activity assays. Effect of naringenin on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway was evaluated by Western blot analysis. BCL2L1 was identified as the candidate target of naringenin against OC. BCL2L1 was upregulated in OC tissues and cells. Naringenin decreased BCL2L1 expression and inactivated the PI3K/Akt pathway in OC cells. Naringenin inhibited cell proliferation and increased the apoptotic rate in OC cells, while these effects were partially abolished by BCL2L1 overexpression and treatment with 740Y-P, a PI3K activator. In conclusion, naringenin exerted an anti-tumor effect on OC progression via inactivation of the PI3K/Akt/BCL2L1 pathway.