Pentagalloylglucose induces ovarian cancer cell senescence via inhibition of AKT signaling
Year: 2026
Type: article
Abstract: This research aimed to investigate the therapeutic potential of pentagalloylglucose (PGG) in ovarian cancer and elucidate its underlying molecular mechanisms. The IC 50 of PGG on A2780, Caov-3, and SK-OV-3 cells was determined using CCK-8 kits. The effects of PGG on cell proliferation, cell cycle, and senescence were assessed by colony formation, EdU staining, flow cytometry, SA-β-gal staining, and γH2AX immunofluorescence. Bioinformatics analysis and molecular docking were employed to predict potential targets of PGG, which were subsequently validated through in vitro and in vivo approaches. A xenograft mouse model was employed to evaluate the anti-tumor activity of PGG in vivo. PGG exhibited cytotoxicity against ovarian cancer cells with IC 50 values of 8.41 µM for A2780, 22.84 µM for Caov-3, and 44.27 µM for SK-OV-3 cells. PGG dose-dependently inhibited proliferation, induced G0/G1 phase arrest, enhanced SA-β-gal and γH2AX positivity, upregulated p16 and p21, and downregulated p-Rb. AKT2 was identified as one of the potential targets. PGG docked into AKT2, promoted its ubiquitination and proteasomal degradation, and inhibited AKT/mTOR signaling. Overexpression of AKT2 reversed PGG-induced growth suppression and senescence promotion. Moreover, PGG effectively inhibited tumor growth in vivo, promoted tumor cell senescence, and suppressed the AKT/mTOR pathway. PGG exerts cytotoxic effects and induces senescence-associated cell cycle arrest in ovarian cancer cells. AKT2 may serve as a key target mediating its anti-ovarian cancer activity. Not applicable.
Source: Cellular Oncology
Institution: Shandong First Medical University
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $4,390
OpenAlex ID: W7225644204
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