Isorhamnetin Induces Melanoma Cell Apoptosis via the PI3K/Akt and NF-κB Pathways

Area of Science:

• Molecular Biology
• Pharmacology
• Oncology

Background:

• Malignant melanoma presents a poor prognosis due to aggressive behavior, drug resistance, and early metastasis.
• Isorhamnetin (IH), a flavonoid, exhibits antitumor properties by inducing apoptosis in various cancer types, but its effect on melanoma is unexplored.

Purpose of the Study:

• To investigate the anti-melanoma effects of Isorhamnetin (IH) in vitro and in vivo.
• To elucidate the molecular mechanisms underlying IH's action against melanoma cells.

Main Methods:

• In vitro studies using B16F10 melanoma cells to assess proliferation, migration, and apoptosis.
• Molecular analysis of signaling pathways, including Akt phosphorylation and NF-κB translocation.
• In vivo experiments to evaluate tumor growth inhibition by IH.

Main Results:

• IH significantly inhibited B16F10 cell proliferation and migration while inducing apoptosis.
• IH suppressed Akt phosphorylation and NF-κB translocation, key mediators in apoptosis.
• The bifunctional enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases 4 (PFKFB4) was identified as a related factor.
• IH demonstrated effective inhibition of tumor growth in vivo.

Conclusions:

• Isorhamnetin (IH) induces apoptosis in melanoma cells both in vitro and in vivo.
• IH's mechanism involves suppressing Akt and NF-κB signaling pathways.
• IH shows promise as a potential therapeutic agent for malignant melanoma.