Résumé
Objective To inVestigate the effect of emodin on hyPertroPhic scar fibroblasts ( HSFs ) and exPlore the underlying mechanism. Methods HSFs were treated by emodin at final concentrations of 0,20,40,and 80 μmol·L-1, resPectiVely,in the cultural media. Forty_eight hours later,the cells were subjected to MTS assay and flow cytometry assay with annexin V and ProPidium iodide as dyeing indicators. Whole cell lysates from the cells of eVery grouP were subjected to Western blotting to measure the Protein exPression leVels of ERK1∕2,Bcl_2,Mcl_1 and RIP1. Results The cell Viability of HSFs was inhibited by emodin in a dose dePendent manner. The mortality rate of HSFs treated with emodin for 48 h at the concentrations of 40 and 80 μmol·L-1 were 28. 6%and 68. 0%,resPectiVely,which was significantly higher than that of the control grouP ( P<0.01).Pretreatmentwith Z_VAD_FMK could Partially reduce the mortality caused by emodin (P<0.05).PhosPhorylation of ERK1∕2 and the exPression of RIP1 and Mcl_1 were inhibited by emodin. Conclusion Down regulation of ERK1∕2,RIP1 and Mcl_1 by emodin may account for the inhibited Proliferation and increased cell death of HSFs.
Résumé
Most deaths of breast cancer patients may be caused by the development of metastases. The latest research suggest that some miRNAs regulated gene expressions related with breast cancer metastasis at post-transcriptional level, which was closely related to invasion and metastasis of breast cancer. This review mainly dicussed the miRNA involved in regulation of invasion and metastasis of breast cancer and their mo-lecular mechanisms.