期刊
ACTA HISTOCHEMICA
卷 123, 期 7, 页码 -出版社
ELSEVIER GMBH
DOI: 10.1016/j.acthis.2021.151793
关键词
MiR-146b-5p; Cholangiocarcinoma cell; Proliferation; TRAF6; P53 translocation
类别
资金
- National Natural Science Youth Foundation of China [81700551]
The study demonstrated that miR-146b-5p is down-regulated in cholangiocarcinoma and functions as a tumor suppressor by inhibiting cell proliferation and promoting cell apoptosis through targeting TRAF6, possibly via modulating p53 translocation to mitochondria.
Background: In view of the poor prognosis and high mortality of cholangiocarcinoma, there is a need for new therapeutic strategies. This study aims to reveal the biological function of miR-146b-5p in cholangiocarcinoma cell and its possible mechanism. Methods: The expression level and prognostic information on miR-146b-5p in cholangiocarcinoma were obtained in TCGA database. The biological function of miR-146b-5p on proliferation and vitality of cholangiocarcinoma cell HUCCT-1 was examined by EdU and MTT assay, and the apoptosis of HUCCT-1 cells transfected with miR146b-5p mimic, mimic control, inhibitor, inhibitor control was detected by flow cytometry analysis. The western blot was done to evaluate the effect of miR-146b-5p targeting substrate and the expression of p53 in whole-cell protein and mitochondria fractions. Results: Our finding revealed that miR-146b-5p expression in patients with CHOL was lower than the normal group(p<0.001). MiR-146b-5p expression was down-regulated in human cholangiocarcinoma HUCCT-1 and RBE cells compared to normal control HIBEC and other cancer cells. The miR-146b-5p mimic could inhibit HUCCT-1 cell proliferation (p<0.05) and promote HUCCT-1 cell apoptosis significantly (p<0.05). The results of western blot showed that miR-146b-5p mimic could directly target TRAF6 3' UTR region and up-regulate the expression of p53 in mitochondria and miR-146b-5p inhibitor could down-regulated the level of p53 in mitochondria. Conclusion: MiR-146b-5p is a cholangiocarcinoma suppressor by inhibiting cell proliferation and promoting cell apoptosis with targeting TRAF6, possibly via modulating p53 translocation to mitochondria.
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