To examine the molecular mechanisms of ferroptosis and cuproptosis in OSCC and explore their potential as therapeutic targets, highlighting their significance in improving treatment outcomes.
Key Findings:
Ferroptosis is distinct from other cell death modalities and is driven by lipid peroxidation, with implications for OSCC treatment.
Cuproptosis induces proteotoxic stress through copper ion interactions with mitochondrial proteins, which may be leveraged for therapeutic strategies.
Both ferroptosis and cuproptosis play roles in OSCC initiation, progression, immune evasion, and therapeutic resistance, highlighting the need for targeted therapies.
Interpretation:
Targeting ferroptosis and cuproptosis may offer novel therapeutic avenues for OSCC, addressing limitations of conventional treatments and potentially improving patient outcomes.
Limitations:
Current understanding of ferroptosis and cuproptosis mechanisms in OSCC is still evolving, particularly regarding their precise roles in tumor biology.
Challenges remain in translating these findings into clinical practice, including the need for robust clinical trials.
Conclusion:
The review highlights the potential of ferroptosis and cuproptosis as therapeutic targets in OSCC, advocating for further research into combination strategies to enhance treatment efficacy.
