Research

The expression of PLK-1 in cervical carcinoma: a possible target for enhancing chemosensitivity

Yuan Zhang^1* , Yu Liu^2* , Yuan-Xian Yang¹ , Jia-Hong Xia³ , Hong-Xiu Zhang⁴ , Hua-Bin Li^3,4 and Chun-Zhao Yu⁴

¹  Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, Hubei, PR China

²  Department of Medicine, Feinberg Medical School, Northwestern University, 745 N Fairbanks, Chicago, IL, USA

³  Department of Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No 1277 Jiefang Avenue, Wuhan, Hubei, PR China

⁴  Department of Surgery, The First Affiliated Hospital, Nanjing Medical University, No 300 Guangzhou Road, Nanjing, Jiangsu, PR China

author email corresponding author email* Contributed equally

Journal of Experimental & Clinical Cancer Research 2009, 28:130doi:10.1186/1756-9966-28-130

Published:	23 September 2009

Abstract

Background

Polo-like kinase-1 (PLK-1) is reported to be upregulated in a variety of human tumors and is implicated in cell proliferation and survival. However, its importance in cervical carcinoma has not yet been fully elucidated.

Methods

We examined PLK-1 expression in cervical carcinoma tissues using immunohistochemical staining. Furthermore, we blocked PLK-1 expression in HeLa cells using specific siRNA and detected the cell cycle, cell proliferation and chemosensitivity using western blotting, MTT and flow cytometry.

Results

We provide evidence that expression of PLK-1 exists in human cervical carcinoma tissues and establish an association with tumor size. Furthermore, we show that PLK-1 knockdown by transfection of siRNA induces accumulation of HeLa cells in the G2/M cell cycle phase and enhances cisplatin-induced apoptosis.

Conclusion

Our results indicate that PLK-1 production in HeLa cells might be critical in determining whether cells survive or undergo apoptosis. Therefore, targeting PLK-1 might be a promising strategy for enhancing sensitivity to chemotherapeutic reagents in cervical carcinoma.