Tuberculosis and Respiratory Diseases  2009;67(4):303-310

doi:10.4046/trd.2009.67.4.303

Relation between Cyclooxygenase-2 and Polo-like Kinase-1 in Non-Small Cell Lung Cancer.

Kyu Hwa LEE 1 ; Seok Chul YANG

Affiliations

+expand

Keywords

Cyclooxygenase 2; Polo-like kinase 1; Lung neoplasms

Country

Republic of Korea

Language

Korean

Abstract

BACKGROUND: Elevated expression of cyclooxygenase-2 (COX-2) and Polo-like kinase-1 (PLK-1) is observed in a wide variety of cancers. Augmented expression of COX-2 and enhanced production of prostaglandin E2 (PGE2) are associated with increased tumor cell survival and malignancy; COX-2 has been implicated in the control of human non-small cell lung carcinoma (NSCLC) cell growth. PLK-1 siRNA induced the cell death of lung cancer cells and the systemic administration of PLK-1 siRNA/atelocollagen complex inhibited the growth of lung cancer in a liver metastatic murine model. COX-2 and PLK-1 are involved in proliferation and in cell cycle regulation, and there is a significant correlation between their interaction in prostate carcinoma. METHODS: In this study, we investigated the pattern of COX-2 and PLK-1 expression in NSCLC, after treatment with IL-1beta, COX-2 inhibitor and PLK-1 siRNA. RESULTS: Expression of PLK-1 was decreased in A549 COX-2 sense cells, and was increased in A549 COX-2 anti-sense cells. Knock out of PLK-1 expression by PLK-1 siRNA augmented COX-2 expression in A549 and NCl-H157 cells. When A549 and NCI-H157 cells were treated with COX-2 inhibitor on a dose-dependent basis, PLK-1 and COX-2 were reduced. However, when the expression of COX-2 was induced by IL-1beta, the production of PLK-1 decreased. CONCLUSION: These results demonstrate that COX-2 and PLK-1 are regulated and inhibited by each other in NSCLC, and suggest that these proteins have a reverse relationship in NSCLC.