Increased the risk of breast carcinoma among older women. Clinic observation on the complication of nifedipine commonly led to mental symptoms and male breast hypertrophy. However, there are other studies showing that CCBs had no relation with cancers. Besides these reports, amlodipine, diltiazem and verapamil were even found to inhibit the growth of breast cancer in themodel of nude mice as well as the meningioma growth. According to the statistics, about 45% of hypertension patients are women. Dihydropyridine e.g. nifedipine accounts for 1/10 of compounds which are daily used in the clinic treatment of hypertension and associated cardiac diseases. It is therefore critical to understand whether CCBs can promote breast cancers and what is the mechanism underlining this cancinoma provocation. In this study, we found and confirmed that nifedipine, but not verapamil, could promote breast cancer both invivo and invitro. Nifedipine decreased miRNA-524-5p, resulting in the up-regulation of brain protein I3. Erk pathway was consequently activated and led to the proliferation and migration of breast cancer cells. Ibrutinib Silencing BRI3 reversed the promoting effect of nifedipine on the breast cancer. In this study, we found that nifedipine significantly stimulated breast cancer growth in the nude mice without any effects on the mice weight. In vivo imaging of tumor tissue in nude mice showed that nifedipine treated mice had stronger and wider range of fluorescence, suggesting tumors were more active and easier to migrate. The pathological section confirmed the hypothesis. CMC-Na groups had complete envelopes and large tumor cells necrosis in the middle of tumors; whereas cancer cells invaded skeletal muscles in the nifedipine treatment groups. Additionally, nifedipine promoted the proliferation and migration of both MDAMB-231 and MCF-7 cells by in-vitro and in-vivo assay. However, verapamil, another calcium channel blocker, didn’t have the similar effects in nude mice. Previous studies have resulted in a controversial conclusion on whether CCBs promote cancer cells. Our results confirmed that nifedipine can potentiate the breast cancers. With respect to the possible mechanism, i modulation was excluded in the first instance. MDA-MB-231 cells don’t express the CACNA1C and CACNA1D subtypes, which is consistent with the previous report. Moreover, that 1 mM nifedipine failed to alter i, ruled out the connection between calcium and the promotion effect of nifedipine. The lack of expression of voltage gated calcium channels in breast cancer cells likely counts upon the rationale that blockers of VGCCs should have no effect on breast cancers. Inconsistent to most previous studies, nifedipine exerts the distinct effect from verapamil, suggesting the specificity of nifedipine on its promotion outcome instead of the character of general blockers of CCBs. Verapamil was even reported to inhibit the growth of cancer cell. Different compound structures and binding motifs may explain the different effects of CCBs on cancer cells. Nifedipine activated the phosphorylation of Erk in MDA-MB-231 cells both invivo and invitro, which suggests it functions through Erk signaling pathway.