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.
ABSTRACT
Objective To explore the effect of vitamin D receptor (VDR) in intestinal tumor development and the relationship between VDR and β-catenin signaling pathway. Methods The interaction of vitamin D receptor and β-catenin were detected by co-immunoprecipitation assay after human colonic carcinoma cells SW480 were treated with vitamin D in vitro for 4 hours. The expression of E-cadherin protein was detected by Western blot after treated for 24 hours. To compare APCmin/+VDR-/- and APCmin/+ mice in vivo, the expression of VDR,β-catenin and BrdU proteins in intestinal tumor were determined by immunohistochemistry. The expression of β-catenin protein in tumor and adjacency intestinal was further determined by Western blot. Results After SW480 cells were treated with vitamin D, vitamin D receptor and β-catenin protein showed binding, the expression of E-cadherin protein further increased (Gray value the control group 145.57±4.21,Gray value of the experimental group 109.35±3.56,t＝32.63,P＜0.05). Immunostaining and Western blot detection（Gray value 166.47±2.36） showed a marked increase of β-catenin level(Gray value 140.51±2.57) in APCmin/+VDR-/- tumor compared to APCmin/+ tumor(145.41±3.62,182.35±3.24,t＝2.65,4.36,P＜0.05). Conclusions The role of vitamin D suppressing intestinal tumor may be achieved through VDR affectingβ-catenin signaling pathway.