The combination of elesclomol and Cu2+ can inhibit the growth of colon cancer cells by targeting FDX1

Abstract

Abstract Background Colon adenocarcinoma (COAD) is the predominant histological type of colon cancer. Elesclomol, a unique copper ion carrier, is considered a potential anticancer drug and has been the subject of a series of clinical trials. FDX1 is the intended target of elesclomol and is believed to be a key regulatory factor in copper-mediated cell death. Through its specific targeting of FDX1, ES-Cu can lead to a reduction in Fe-S stability, potentially enabling more precise tumor destruction. However, further research is still needed regarding the use of elesclomol in the treatment of colon adenocarcinoma. Methods Through bioinformatics analysis, this study aims to explore the molecular expression, clinical relevance, and prognostic significance of FDX1 in COAD Additionally, based on in vitro and in vivo experiments, the therapeutic value of elesclomol in the treatment of colon adenocarcinoma will be investigated. Result The expression of FDX1 is significantly different between COAD and normal tissues. Patients with high expression of FDX1 tend to have better prognosis compared to those with low expression. FDX1 shows high sensitivity and specificity in diagnosing colon cancer. Immunohistochemical analysis suggests a strong correlation between FDX1 and various immune cells and immune checkpoints. TIDE scoring also indicates that patients with high FDX1 expression levels are more responsive to immune therapy. Furthermore, both in vitro and in vivo experiments have demonstrated that the combination of elesclomol and Cu2 + efficiently inhibits the growth of colon cancer cells, and the safety profile of this treatment approach is acceptable. Lastly, real-time quantitative PCR (qRT-PCR) experiments on colon cancer cell lines and animal tumor models have shown that elesclomol upregulates the expression level of FDX1. Conclusion The combination of elesclomol and Cu2 + can inhibit the growth of colon cancer cells by targeting FDX1.