〔Abstract〕 Objective To investigate the effect of interference with AKAP12 on the proliferation ability of human breast cancer MCF-7 cells and to explore its mechanism. Methods MCF-7 cells were exogenously transfected lentivirus with shRNA-AKAP12 and shRNA-NC, respectively. Western blot was conducted to examine the expression of AKAP12 protein in transfected cells. The proliferation ability of transfected cells were measured by CCK-8 assay and cell plate cloning assay. Western blot was used to detect the protein expression levels of cyclin-dependent kinase(CDK) inhibitors(p21, p27) and cell cycle progression-related CyclinD1. Results Compared to shRNA-NC cells, the expression of AKAP12 protein in shRNA-AKAP12 cells decreased. CCK-8 assay and colony formation assay showed that the cell proliferation ability of shRNA-AKAP12 cells increased significantly(P<0.000 1,P<0.001). Compared to the shRNA-NC cells, the expression of the cyclin-dependent kinase(CDK) inhibitors(p21, p27) were down-regulated in the shRNA-AKAP12 cells, while the cell cycle progression protein(CyclinD1) was up-regulated. Conclusion The study indicated that interference with AKAP12 gene could increase the proliferation ability of MCF-7 cells. It accelerated the G1-S phase transition of MCF-7 cells after interference with AKAP12 gene. Thus it is available to clinical treatment and prognosis evaluation of estrogen receptor-positive breast cancer.