Friedelin induces apoptosis in oral cancer: Insights from in vitro and in silico studies

Area of Science:

• Natural product chemistry
• Molecular oncology
• Cancer biology

Background:

• Oral cancer presents significant global health challenges with high mortality.
• Dysregulated apoptosis contributes to oral cancer progression and treatment resistance.
• Friedelin, a triterpenoid, shows promise in modulating apoptosis pathways.

Purpose of the Study:

• To investigate the therapeutic potential of Friedelin against oral cancer.
• To examine Friedelin's interaction with apoptotic proteins.
• To assess Friedelin's cytotoxic effects and apoptosis-inducing capabilities in oral cancer cells.

Main Methods:

• Constructed interaction networks using CTD, GeneCards, and STITCH databases.
• Performed molecular docking to determine binding affinities with apoptotic proteins.
• Conducted in vitro assays (MTT, morphology, Annexin V-FITC) for cytotoxicity.
• Validated apoptosis regulation via gene expression analysis.

Main Results:

• Identified key interactions between Friedelin and apoptotic regulators.
• Demonstrated strong binding of Friedelin to Bax (-8.3 kcal/mol) and Bcl2 (-8.0 kcal/mol).
• Observed dose- and time-dependent cytotoxic effects and confirmed apoptosis induction via intrinsic pathways (upregulation of Bax, Caspase-3, TP53; downregulation of Bcl2).

Conclusions:

• Friedelin exhibits potential as an anticancer agent for oral cancer by inducing apoptosis.
• Friedelin modulates apoptotic signaling pathways, offering a novel therapeutic strategy.
• Further in vivo validation and clinical translation are warranted for Friedelin.