Objective To study the expression and the function of DKK2 and to explore its potential mechanisms in breast cancer.Methods The expression of DKK2 was detected by RT-PCR in normal breast tissues and breast cancer cells.we have transfected DKK2 into breast cancer cell lines MDA-MB-231 and MCF-7.The cells before transfection were used as control group and marked with Vector.The cells after transfection were used as experimental group and marked with DKK2.Furthermore by qRT-PCR and Western-blot,the expression of DKK2,Notch signaling pathway and related factors were analyzed.We also detected the function of DKK2 by cloning assay,Transwell assay and proliferation assay.Results No expression of DKK2 was found in breast cancer cell lines MDA-MB-231 or MCF-7,with relatively high expression in normal breast tissue.The number of apoptotic cells was 2.57±1.18 before transfectionin in cell line MDA-MB-231,and 49.53±8.27 after transfection.The difference was statistically significant between the two groups (P＜0.005).The relative colony formation rate of MDA-MB-231 cells and MCF7 cells after transfection accounted for 20.44％ and 15.21％,respectively.The difference was statistically significant by t test.The number of apoptosis cells in MB231/DKK2 group was 49.53± 8.27 and that in MB231 / Vector group was 2.57±1.18.The difference was statistically significant (P＜0.005).The number of migrated cells in MB231/DKK2 group was 112.0±8.1 and that in MB231/Vector group was 178.0±12.0.The difference was statistically significant (P＜0.005).The mRNA expression of Notch 1 in group MB231/Vector was recorded as 1.The mRNA expression of JAG1 in MB231/DKK2 group was 0.2891.The difference was also statistically significant (P＜0.005).Conclusions Restored expression of DKK2 in silenced breast cells suppresses breast cancer cell proliferation and migration through repressing Notch signaling.DKK2-Notch signaling pathway may be its potential molecular mechanism to function in breast cancer.DKK2 may be one of the target genes for early diagnosis and treatment of breast cancer.

Botulinum toxin(BoNT)is currently the first-line method for treating focal dystonia,which causes muscle paralysis by chemical denervation.Recent neuroimaging studies have found that BoNT treatment could alter neuroplasticity in the brain of patients with focal dystonia.However,the specific central nervous system mechanisms have not been fully elucidated.To this end,here we review the neuroimaging studies on BoNT treatment for dystonia from three aspects:functional magnetic resonance imaging,structural magnetic resonance imaging,and positron emission tomography imaging.It suggests that BoNT may improve the symptoms of dystonia patients by affecting functional connectivity,microstructure,and metabolic levels of the cortex,basal ganglia,thalamus,and cerebellum,etc.Therefore,this review will provide a theoretical reference for further exploring the mechanism and developing potential therapeutic targets of dystonia.