Nuclear Receptors as Potential Pharmacological Targets for Colorectal Cancer Therapy via Regulating Wnt/β-catenin Signaling

Hyperactivation of the Wnt/β-catenin signaling pathway due to mutations in its components initiates the majority of colorectal cancer (CRC) cases and promotes CRC development. Unphosphorylated β-catenin accumulates in the nuclear and interacts with TCF/LEF factors to stimulate the transcription of the downstream target genes of Wnt/β-catenin signaling. Therefore, the suppression of dysregulated Wnt/β-catenin signaling is considered as a promising strategy for CRC therapy. In the past decade, accumulating evidence revealed that nuclear receptors (NRs) modulated Wnt/β-catenin signaling activity via binding to diverse members of this pathway. In this review, we mainly focus on the regulation and the underlying mechanisms of Wnt/β-catenin signaling by NRs and their ligands or pharmacological modulators. Their potential in the precise treatment and individualized therapy for colorectal cancer is also discussed.