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Retinoid X receptor α ( RXR α) plays important roles in the malignancy of several cancers such as human prostate tumor, breast cancer, and thyroid tumor. However, its exact functions and molecular mechanisms in cholangiocarcinoma ( CCA ), a chemoresistant carcinoma with poor prognosis, remain unclear. In this study we found that  RXR α was frequently overexpressed in human  CCA  tissues and  CCA  cell lines. Downregulation of  RXR α led to decreased expression of mitosis‐promoting factors including cyclin D1and cyclin E, and the proliferating cell nuclear antigen, as well as increased expression of cell cycle inhibitor p21, resulting in inhibition of  CCA  cell proliferation. Furthermore,  RXR α knockdown attenuated the expression of cyclin D1 through suppression of Wnt/β‐catenin signaling. Retinoid X receptor α upregulated proliferating cell nuclear antigen expression through nuclear factor‐κB ( NF ‐κB) pathways, paralleled with downregulation of p21. Thus, the Wnt/β‐catenin and  NF ‐κB pathways account for the inhibition of  CCA  cell growth induced by  RXR α downregulation. Retinoid X receptor α plays an important role in proliferation of  CCA  through simultaneous activation of Wnt/β‐catenin and  NF ‐κB pathways, indicating that  RXR α might serve as a potential molecular target for  CCA  treatment.

Retinoid X receptor α enhances human cholangiocarcinoma growth through simultaneous activation of Wnt/β‐catenin and nuclear factor‐κB pathways