Prediction of new targets and mechanisms for quercetin in the treatment of pancreatic cancer, colon cancer, and rectal cancer.

Quercetin has been widely found to exhibit anticancer activity with low toxicity and prevalence in foods. Quercetin has been reported to inhibit digestive system cancers including pancreatic cancer (PAAD) and colon cancer (COAD), but rectal cancer (READ) has not been reported. The reported mechanisms and targets are divergent. In this study, new targets and mechanisms were predicted for the influence of quercetin on PAAD, COAD, and READ using bioinformatics methods. The results showed that quercetin may target CD36 and reduce the death rate caused by PAAD by enhancing the cell adhesion, mediating the uptake of fatty acids (FAs), regulating thrombospondin-1, and stimulating the immune response. Quercetin may lower the death rate from READ by targeting SLCO1B1 and producing enhanced effects from use of this compound, inhibiting cell growth, and inducing apoptosis in tumor cells. ACADS, ALDH3B2, UGT2A3, AMH, CDKN2A, FOSL1, CD36, CFL2, CYP3A4, and MAF were identified as targets for quercetin to reduce the death rate caused by COAD. Glutathione metabolism was mainly involved in the effect of quercetin on COAD, including the enhancement of the oxidation of fatty acids, the metabolism of anticancer medications, and the stiffness of cells, and the reduction of chemical carcinogenesis, the level of anti-Müllerian hormone, the proliferation of cancer cells and transcriptional misregulation, and mediation of the activity of glutathione transferases. The combined analyses of three databases can be referred to and used to seek medications and targets that can be applied to other diseases.