Abstract: Objective To investigate the effect of p55PIK on cell cycle and proliferation of breast cancer cells MCF7, and the potential mechanism. Methods Breast cancer cells MCF7 were transfected with plasmids or specific siRNA for over-expression or low-expression of p55PIK. Then p55PIK expression was detected by Western blot. Cell cycle and DNA synthesis were measured through BrdU/PI. Meanwhile, Cell Counting Kit-8(CCK-8) assay was performed to detect the proliferation of breast cancer cells MCF7, and a co-immunoprecipitation assay was conducted to find out whether p55PIK could bind with proliferating cell nuclear antigen(PCNA). Results p55PIK was successfully up-regulated or down-regulated after transfection. p55PIK overexpression could promote DNA synthesis and the proliferation of breast cancer MCF7 cells DNA synthesis by BrdU: p55PIK vs. Vector, (56.33±1.63)% vs. (26.27±1.85)%, P<0.01; CCK-8 at OD450nm: p55PIK vs. Vector, (1.46±0.04) vs. (1.16±0.16), P<0.05). Meanwhile, down-regulation of p55PIK could inhibit cell cycle and the proliferation of breast cancer cells MCF7. p55PIK could combine with PCNA. Conclusion p55PIK could promote cell cycle progress and the proliferation of breast cancer cells MCF7. Moreover, p55PIK could combine with PCNA.