Apigenin inhibits recurrent bladder cancer progression by targeting VEGF-β

Area of Science:

• Oncology
• Molecular Biology
• Biochemistry

Background:

• Bladder cancer, including muscle-invasive (MIBC) and recurrent non-muscle-invasive (NMIBC) types, poses significant global health challenges.
• The therapeutic mechanisms of apigenin, a promising natural flavonoid for bladder cancer, are not fully understood.
• Identifying novel therapeutic targets is crucial for improving bladder cancer treatment outcomes.

Purpose of the Study:

• To elucidate the therapeutic mechanism of apigenin in bladder cancer.
• To identify potential drug targets for apigenin in bladder cancer treatment.
• To investigate the role of VEGF-β in bladder cancer progression and its interaction with apigenin.

Main Methods:

• Single-cell RNA sequencing (scRNA-seq) for differential gene expression analysis.
• Drug target screening to identify common targets between apigenin and bladder cancer.
• Molecular docking to assess apigenin's binding affinity with VEGF-β.
• In vitro assays to validate the functional role of VEGF-β and apigenin's effects.

Main Results:

• 51 common targets between apigenin and bladder cancer were identified, with VEGF-β being a dominant gene.
• Molecular docking confirmed a strong binding affinity between apigenin and VEGF-β.
• VEGF-β was significantly upregulated in fibroblasts from recurrent bladder cancer, correlating with malignancy and promoting tumor progression.
• Apigenin demonstrated significant inhibition of bladder cancer progression by targeting VEGF-β in vitro.

Conclusions:

• VEGF-β is a key mediator in bladder cancer progression and a potential diagnostic marker.
• Apigenin effectively targets VEGF-β, showing promise as a chemopreventive and therapeutic agent for recurrent bladder cancer.
• Targeting VEGF-β offers a potential therapeutic strategy for managing bladder cancer.