The P7 peptide antagonizes bFGF-induced malignant behaviors of ovarian cancer by inhibiting MEK/ERK signaling pathway

Background: Ovarian Cancer (OC) is a highly invasive malignancy with poor prognosis, underscoring the need for novel therapeutic strategies. Basic Fibroblast Growth Factor (bFGF) promotes OC progression by activating the MEK/ERK signaling pathway, enhancing tumor cell proliferation, migration, and invasion. P7 peptide is a novel peptide with potential antitumor effects, though its mechanism of action remains unclear. This study investigates whether P7 peptide inhibits bFGF-induced OC progression via suppression of the MEK/ERK pathway.

Methods: Human OC Anglne cells were treated with varying concentrations of bFGF and P7 peptide. Cell proliferation was measured using CCK-8 assays, while RT-PCR and Western blot analyses evaluated the expression of uPA, MMP2, and E-cadherin, along with MEK/ERK pathway activation. Cell migration and invasion were assessed via wound healing and Transwell assays.

Results: bFGF (30 ng/mL, 48 h) significantly enhanced cell proliferation and invasive behavior, alongside upregulation of uPA and MMP2 and reduced E-cadherin expression. P7 peptide (16 μM, 48 h) effectively reversed these effects and inhibited MEK/ERK phosphorylation.

Conclusion: These findings suggest that P7 peptide suppresses bFGF-mediated OC progression by targeting the MEK/ERK pathway, supporting its potential as a novel therapeutic agent in OC.

MEK/ERK signaling pathway; Ovarian cancer; P7 peptide; basic fibroblast growth factor; cell migration and invasion.