PKCξ, MMP-2 and MMP-9 expression in lung adenocarcinoma and association with a metastatic phenotype

Abstract

The aim of the present study was to investigate protein kinase C-type (PKCξ), matrix metalloproteinase (MMP)-2 and MMP9 expression in lung adenocarcinoma and to define their association with in vitro invasion and metastatic capacity. PKCξ, MMP-2 and MMP-9 expression was assessed by immunohistochemistry in 110 cases of lung adenocarcinoma. PKCξ small interfering (si)RNA was transfected into A549 cells, and western blotting was used to confirm PKCξ-knockdown in transfected cells and to measure MMP-2 and MMP-9 levels. A Transwell invasion assay was used to detect in vitro invasive capacity. The rates of positive PKCξ MMP-2 and MMP-9 staining in lung adenocarcinoma tissues were 52.73, 55.45 and 61.82%, respectively. PKCξ expression was increased in malignant tissues compared with adjacent normal lung tissues and was associated with lymph node metastasis (P<0.05), although it was not associated with any other clinicopathological parameters, including sex, age, tumor size, smoking status or distant metastases (all P>0.05). PKCξ, MMP-2 and MMP-9 expression was markedly decreased in siPKCξ-treated A549 cells, which exhibited a significantly decreased invasive capacity in the Transwell invasion assay (P<0.05). In conclusion, PKCξ promoted lung adenocarcinoma invasion and metastasis, and its expression was associated with MMP-2 and MMP-9 expression. PKCξ may be a potential target for gene therapy in lung adenocarcinoma.