ABSTRACT
@#Ferroptosis is a newly discovered method of programmed cell death. Current studies have shown that activation of ferroptosis-related pathways can inhibit the growth and proliferation of tumor cells and reverse their drug resistance. Oral cancer is a common malignant tumor with a high recurrence rate and high drug resistance. Inducing ferroptosis is a potential treatment strategy. There are still many uncertainties in the application of ferroptosis in the treatment of oral cancer, which need to be further explored. This article systematically introduces the mechanism of ferroptosis and its recent progress in oral cancer treatment to provide new mechanisms and methods for the clinical treatment of oral cancer. Current research shows that the mechanism of ferroptosis is mainly related to amino acid metabolism, Fe2+ metabolism, and lipid metabolism. Ferroptosis in oral cancer cells can reverse drug resistance in cancer cells and improve the activity of immune cells. New drugs, such as curcumin analogs and triptolide, can induce ferroptosis in oral cancer, and the development of nanomaterials has improved the utilization rate of drugs. Inhibiting the expression of the ferroptosis-related factors SLC7A11, NF-E2-related factor 2 (Nrf2), and ferritin heavy chain 1 (FTH1) can promote ferroptosis in oral cancer cells. It is a potential target for the clinical treatment of oral cancer, but its translation into clinical practice still needs further research.
ABSTRACT
Objective @#To investigate the expression of brain expressed X-linked gene 1(Bex1) and nuclear factor-kBp65 (NF-kBp65) in tongue squamous cell carcinoma, and its significance.@*Methods@# Immunohistochemistry was used to detect the expression of Bex1 and NF-kBp65 in 60 tongue squamous cell carcinoma (TSCC) tissues and adjacent normal tissues, and the relationships between Bex1, NF-kBp65 and the clinicopathological features and prognosis of patients were analyzed.@*Results @#The positive expression rate of Bex1 in TSCC was 48.3% (29/60), which was significantly lower than that in adjacent normal tissues 88.3% (53/60) (x2=22.18, P < 0.01). The positive rate of Bex1 was negatively correlated with TNM stage, and the difference was statistically significant (P < 0.05). The positive rate of 63.3% (38/60) in TSCC was significantly higher than 20% (12/60) in adjacent normal tissues (x2=23.18, P < 0.01), the positive rate of NF-kBp65 was positively correlated with TNM stage, and the difference was statistically significant (P < 0.05). According to the Pearson correlation analysis results, the expression of Bex1 and NF-kBp65 in TSCC tissues was negatively correlated (r=-0.302, P=0.019). Kaplan-Meier survival curves showed that the survival rate of Bex1 positive patients was significantly higher than that of Bex1 negative patients.@*Conclusion @#In TSCC tissues, the low positive expression rate of Bex1 and the high positive expression rate of NF-kBp65 may promote tumor invasion and metastasis, and the negative expression of Bex1 may be related to the poor prognosis of patients.