Objective To investigate the effect of microRNA-584-5p (miR-584-5p) on the biological behavior (proliferation, migration and invasion) of breast cancer cells and its mechanism. Methods Human normal breast epithelial cells MCF10A and breast cancer cells MDA-MB-231, SK-BR-3 and MCF-7 were selected; take MCF-7 cells in logarithmic growth phase, transfect them with LipofectamineTM 2000 transfection kit, and divide them into seven groups: blank group (untransfected MCF-7 cells), mimic-negative control (mimic-NC) group (transfected mimic-NC), miR-584-5p mimic group (transfected miR-584-5p mimic), pcDNA group [transfected with overexpression of matrix metalloproteinase-14 (MMP-14) pcDNA3.1 plasmid negative control (pcDNA3.1)], MMP-14 group [transfected with overexpression of MMP-14 pcDNA3.1 plasmid (pcDNA3.1-MMP-14)], mimic-NC+MMP-14 group (co-transfected with mimic NC and pcDNA3.1-MMP-14), and miR-584-5p mimic+MMP-14 group (co-transfected with miR-584-5p mimic and pcDNA3.1-MMP-14). The mRNA expression levels of miR-584-5p in MCF10A, MDA-MB-231, SK-BR-3 and MCF-7 cells and the expression levels of miR-584-5p and MMP-14 mRNA of MCF-7 cell in each group were detected by fluorescence quantitative PCR. The protein expressions of MMP-14 of MCF-7 cell in each group were detected by Western blotting. The proliferation, migration and invasion of MCF-7 cell in each group were detected by cell counting kit - 8 (CCK-8), scratch test and Transwell test. The targeting relationship between miR-584-5p and MMP-14 was detected by double luciferase reporter gene assay. Results Compared with the human normal mammary epithelial cells MCF10A, the expression levels of miR-584-5p in breast cancer cells MDA-MB-231, SK-BR-3 and MCF-7 were decreased (P<0.05), and the expression level of miR-584-5p in MCF-7 cells was the lowest. Compared with the blank group and the mimic-NC group, the expression level of miR-584-5p of MCF-7 cells in the miR-584-5p mimic group was increased, and the expression levels of MMP-14 mRNA and protein, proliferation activity, scratch healing rate and invasive cell number were decreased or reduced (P<0.05). Compared with the blank group and the pcDNA group, the expression levels of MMP-14 mRNA and protein, proliferation activity, scratch healing rate and invasive cell number of MCF-7 cells in the MMP-14 group were increased (P<0.05). Compared with the MMP-14 group and the mimic-NC+MMP-14 group, the expression level of miR-584-5p of MCF-7 cells in the miR-584-5p mimic+MMP-14 group was increased, the expression levels of MMP-14 mRNA and protein, proliferation activity, scratch healing rate and invasive cell number were decreased or reduced (P<0.05). The expression levels of MMP-14 mRNA and protein, proliferation activity, scratch healing rate and invasive cell number of MCF-7 cells in the miR-584-5p mimic+MMP-14 group were higher or morer than those in the miR-584-5p mimic group (P<0.05). The results of double luciferase reporter gene test showed that miR-584-5p could targeted action on the MMP-14 promoter region. Conclusions MiR-584-5p can targetable regulate the expression of MMP-14. Overexpression of miR-584-5p inhibits the proliferation, migration and invasion of breast cancer cells by down-regulating MMP-14.
ObjectiveTo understand the clinical value of centromere proteins (CENPs) in hepatocellular carcinoma and their influence on the malignant biological behavior of hepatocellular carcinoma, and to provide theoretical references for related research in this field. MethodDomestic and international databases were searched for relevant literatures on the study of CENPs in hepatocellular carcinoma in recent years to be analyzed and reviewed. ResultsA total of 11 CENPs closely related to hepatocellular carcinoma had been summarized, which were differentially expressed in hepatocellular carcinoma and correlated with prognosis. CENPs might regulate various malignant biological behaviors such as hepatocellular carcinoma proliferation, metastasis, apoptosis, and resistance to radiotherapy and thus participate in the development of hepatocellular carcinoma via multiple mechanisms. The roles and mechanisms of some CENPs in hepatocellular carcinoma remained unclear. ConclusionsCENPs play an essential role in the diagnosis, treatment, and prognosis of hepatocellular carcinoma. They are involved in multiple malignant biological behaviors of hepatocellular carcinoma and are expected to be potential therapeutic targets for hepatocellular carcinoma. However, their roles and mechanisms in hepatocellular carcinoma remain to be investigated.