Among them, SMOC1, KCNC4, PDE4DIP and COL14A1 have been reported to associate with a variety of tumors. SMOC1 is SPARC related modular calcium binding 1 and has been found a correlation with malignant progression, such as brain tumor, colorectal cancer and breast cancer. KCNC4 is a potassium voltage-gated channel and the expression increase of Kv3.4 can promote the proliferation of OSCC. PDE4DIP is a tumor marker for diagnose and establish a prognosis in patients with esophageal squamous cell carcinoma. COL14A1 may be involved in the basement membrane regulation, providing specific molecular bridges between fibrils and other matrix components. However, our work revealed that BRI3 is closely related with this SAR131675 nifedipine effect on breast cancers. BRI3 participates in tumor necrosis factor- induced cell death. Silencing of BRI3 expression clearly suppressed the phosphorylation of Erk, and consequently the proliferation and migration of MDA-MB-231 cells, suggesting that the BRI3-Erk signaling pathway is involved in regulation of this nifedipine effect on breast cancers. As another mechanism underlining nifedipine promoting the breast cancer cell migration, up-regulation of ANGPTL7 was found in response to the nifedipine treatment. ANGPTL7 is a member of angiopoietin family as vascular regulators which functions as a general endothelial cell survival factor and modulates endothelial cell adhesion. Previous work has shown that ANGTL can cause the gap between endothelial cells resulting in the metastasis of breast cancers. MicroRNAs are small, single-stranded, non-coding RNAs that regulate gene expression. Their dysregulation therefore contributes to cancer cells’ proliferation and migration. For example, miRNA-10b initiated breast tumor invasion and metastasis. miRNA-135a promoted breast cancer cell migration and invasion by targeting HOXA10. Restoration of miRNA-145 suppresses prostate cancer cell proliferation, migration and invasion by targeting FSCN1. In our study, expression of miRNA-524-5p decreased after cells were treated with nifedipine and miRNA-524-5p regulated the expression of BRI3 gene. Thus the effects of nifedipine on breast cancer is carried out by miRNA-524-5pBRI3–Erk signaling pathway. The women occupy about 1/3 in all the hypertension patients. Some of them are suffering or are genetically easier to develop breast cancers. Thus it is urged that prescription of nifedipine to women should be seriously caution. Nifedipine is dangerous for patients with breast cancers and it may worsen the situation. As a result, doctors should be aware of the fact that nifedipine promotes the breast cancers and avoid nifedipine for the women especially who suffer both breast cancer and hypertension. The deposition of Ab in the brain is a principal target in many AD treatment strategies. A current hot topic in the field is using immunotherapy to reduce and eliminate Ab deposition. The concomitant reduced b-amyloid burden is associated with restored cognitive function. The Ab vaccine has been shown to decrease and eliminate Ab deposition in the brains of AD transgenic mice and to impair behavioral and cognitive disorders in experimental mice.