Lentivirus-mediated knockdown of CEP55 suppresses cell proliferation of breast cancer cells

Abstract

Centrosomal protein 55 (CEP55), as a microtubule-bundling protein, plays an important role in cell cycle regulation. CEP55 has been recognized recently in several human cancers. In this study, we first observed that the mRNA level of CEP55 is commonly up-regulated in breast cancer compared with their normal counterparts as demonstrated by data derived from Oncomine database. To further evaluate the functional role of CEP55 in breast cancer cells. Expression of CEP55 was efficiently knocked down using lentivirus-mediated RNA interference in human breast cancer cell line ZR-75-30, as evidenced by quantitative real-time PCR (qRT-PCR) and Western blot analysis. Further investigations revealed that CEP55 knockdown significantly inhibited cell proliferation and colony formation. Moreover, flow cytometer analysis indicated knockdown of CEP55 induced cell cycle arrested at G0/G1 phase and cell apoptosis. These findings suggest that CEP55 plays a crucial role in promoting breast cancer cell proliferation and it might be a potential therapeutic target in breast cancer.