Abstract: Objective　To investigate the effect of baicalin (BC) on the proliferation of human cholangiocarcinoma (CCA) cell lines, QBC939 and RBE, and its underlying mechanism thereof. Methods　QBC939 and RBE cells on logarithmic growth phase were treated with different concentrations of BC for 24 h, and CCK-8 was used to evaluate the effect of BC alone treatment or in combination with c-Myc knockdown on the cell proliferation activity. The effect of BC on cell growth status was observed by microscope in CCA cells. The effect of BC on the cell cycle was examined by flow cytometry. Western blot assay was also employed to detect the effects of BC and c-Myc knockdown mediated by siRNA on the expressions of cell cycle related proteins, such as cyclin-dependent kinase inhibitor p27, Cyclin D1 and proto-oncogene protein c-Myc, respectively. Results　BC significantly inhibited the proliferation activities of QBC939 and RBE cells compared with 0 μmol/L group (P＜0.01). BC-treated cells were slow growth observed under the microscopic. BC significantly induced cell cycle arrest in S phase in QBC939 cells (P＜0.05). The protein levels of p27 and Cyclin D1 were markedly increased and decreased, respectively with the increase of BC concentrations (P＜0.01). The protein level of c-Myc was also declined after BC treatment. The knockdown of c-Myc alone with siRNAs demonstrated a same change in the protein levels of p27 and Cyclin D1 compared to BC treatment in QBC939 and RBE cells (P＜0.05). The knockdown of c-Myc alone can significantly inhibit the proliferation activities of QBC939 and RBE cells and further enhance the inhibitory effect of BC (P＜0.01). Conclusion　BC inhibits the proliferation of CCA cells via blocking c-Myc signaling pathway. 

Key words: Baicalin, cell proliferation, cell cycle, cyclin-dependent kinase inhibitor p27, Cyclin D1, proto-oncogene proteins c-Myc, cholangiocarcinoma, RNA, small interfering