Several pathways including Wnt/β-catenin, Hedgehog, and Notch have been identified to be critical to the self-renewal behavior of CSCs. Furthermore, CSCs have been suggested to contribute to tumor resistance/relapse because chemotherapy and radiation therapy are incapable of eradicating them. Thus, targeting these selfrenewal pathways may provide an effective strategy to target CSCs and thereby overcome tumor resistance and reduce relapse. Several dietary compounds, such as curcumin, quercetin, and epigallocatechin-gallate, were found to be potentially against CSC self-renewal.
Several molecular markers have been identified for the characterization of colorectal CSCs, including surface molecules such as CD133, CD44, CD24, LGR5, and EpCAM2,9–15 and drug efflux transporters like ALDH1 and ABCG216–19. Among those markers, CD24, CD44, LGR5, and ALDH1 are target genes of Wnt/β-catenin signaling as well as key hallmarks of colorectal CSCs. Emerging data suggest that the Wnt signaling is essential to colorectal CSC function and that β-catenin-mediated regulation of target genes is closely related to colorectal cancer malignancy. [2]