Baicalin induces ferroptosis in oral squamous cell carcinoma by suppressing the activity of FTH1

Area of Science:

• Oncology
• Molecular Biology
• Biochemistry

Background:

• Oral squamous cell carcinoma (OSCC) is a significant global health concern.
• Ferroptosis, a regulated cell death pathway, is implicated in cancer development.
• The role of ferroptosis-related genes (FRGs) in OSCC remains incompletely understood.

Purpose of the Study:

• To investigate the role of the ferroptosis-related gene FTH1 in OSCC.
• To evaluate the therapeutic potential of baicalin in OSCC treatment.
• To establish a prognostic model for OSCC based on FRGs.

Main Methods:

• Bioinformatic analysis to develop a 12-FRG prognostic model for OSCC.
• Immunohistochemistry and bioinformatic characterization of FTH1 expression in OSCC samples.
• In vitro assays (wound healing, Transwell, Western blotting, EdU) to assess FTH1's impact on cell migration, invasion, EMT, and proliferation.
• Ferroptosis marker analysis and Mito Tracker staining to evaluate FTH1-mediated ferroptosis.
• Assessment of baicalin's therapeutic effects on OSCC cells, focusing on FTH1, ferroptosis, proliferation, and EMT.

Main Results:

• A 12-FRG prognostic model identified FTH1 as significantly upregulated in OSCC and associated with prognosis, immune infiltration, and drug sensitivity.
• FTH1 knockdown inhibited OSCC cell proliferation, epithelial-mesenchymal transition (EMT), and invasion, while inducing ferroptosis.
• Baicalin directly suppressed FTH1 expression in OSCC cells, promoting ferroptosis and inhibiting proliferation and EMT.

Conclusions:

• FTH1 is a potential therapeutic target for oral squamous cell carcinoma.
• Baicalin demonstrates promising therapeutic potential for OSCC by targeting FTH1 and inducing ferroptosis.