ABSTRACT
The breast cancer is the most common malignant tumor of women, and its treatments were widely explored.A lot of studies have confirmed that the abnormal activation of WNT/ beta-catenin signaling pathway and the abnormal expression of miRNA are closely related to the occurrence and development of breast cancer.miRNA could target the regulation of WNT/beta-catenin signaling pathway and affect the occurrence and development of many human tumors as an endogenous non-coding small molecule RNA.Therefore, the mechanism of WNT/beta-catenin signaling pathway in breast cancer and its interaction with miRNA may provide new ideas for the treatment of breast cancer.The article reviewed the composition of the WNT/beta-catenin signaling pathway and the role of this signaling pathway and its interaction with miRNA in the pathogenesis and progression of breast cancer.
ABSTRACT
Objective To investigate the impact of triptolide (TP) on proliferation and apoptosis of imatanib resistant CML cell (K562/G01) and its regulating effect on Wnt/β3-catenin signal pathway.Methods A series of 10,20,40,and 80 nmol/L of triptolide were used in CML cells K562/G01 for 12,24,and 48 hours.The cell proliferation was detected with methyl thiazolyl tetrazolium (MTT) test.The apoptosis was assessed with flow cytometry (FCM).The mRNA expressions of breakpoint cluster region-c-abl (BCR-ABL),β-catenin and its down-stream targets Lef-1,and cyclinD1 were analyzed with real-time quantitative polymerase chain reaction (RT-PCR),respectively.Results Triptolide significantly inhibited K562/G01 cell growth ability and induced apoptosis in a dose-dependent manner.Mter being treated with 20,40 nmol/L TP for 24 hours,the cell growth inhibition rates were (22.62 ± 1.33) ％,and (51.41 ±1.39) ％,respectively.The late apuptosis rates were (6.91 ± 0.14) ％,and (7.64 ± 0.47) ％,respectively.Meanwhile,PCR data showed that the mRNA levels of BCR-ABL were decreased,compared to the control group,the mRNA levels of β-catenin,Lef-1,and cyclinD1 were also decreased obviously after treatment.Conclusions Our data indicated that the triptolide could inhibit the proliferation and induce the apoptosis of K562/G01,and the mechanism might be related to the blockade of Wnt/β-catenin signal pathway.