Nitidine chloride efficiently induces autophagy and apoptosis in melanoma cells via AMPK-mTOR signaling pathway

Area of Science:

• Oncology
• Molecular Biology
• Cell Biology

Background:

• Nitidine chloride (NC) demonstrates anti-tumor properties across various cancers.
• The specific impact of NC on human melanoma remains largely uncharacterized.

Purpose of the Study:

• To investigate the anti-cancer effects of NC on human melanoma cell lines A375 and WM35.
• To elucidate the mechanisms of NC-induced cell death, focusing on apoptosis and autophagy.

Main Methods:

• Cell proliferation was assessed using MTT assays.
• Apoptosis was evaluated by measuring caspase-3 activity and protein levels.
• Autophagy was analyzed via transmission electron microscopy (TEM), immunostaining, and immunoblotting.
• The AMPK-mTOR pathway's role was investigated.

Main Results:

• NC significantly inhibited proliferation in A375 and WM35 melanoma cells.
• NC induced apoptosis, evidenced by increased caspase-3 activity and expression.
• NC triggered autophagy and activated the AMPK-mTOR pathway.
• Inhibiting autophagy (using 3-MA) or the AMPK pathway amplified NC-induced apoptosis and cell death.

Conclusions:

• NC exhibits potent anti-melanoma effects by inducing apoptosis and autophagy.
• NC-induced autophagy may confer a cytoprotective role in melanoma cells.
• Targeting NC-induced autophagy could be a therapeutic strategy for melanoma.