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

The aim of the present study was to investigate protein kinase C zeta type (PKC zeta), matrix metalloproteinase (MMP)-2 and MMP-9 expression in lung adenocarcinoma and to define their association with in vitro invasion and metastatic capacity. PKC zeta, MMP-2 and MMP-9 expression was assessed by immunohistochemistry in 110 cases of lung adenocarcinoma. PKC zeta small interfering (si) RNA was transfected into A549 cells, and western blotting was used to confirm PKC zeta-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 PKC zeta, MMP-2 and MMP-9 staining in lung adenocarcinoma tissues were 52.73, 55.45 and 61.82%, respectively. PKC zeta 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). PKC zeta, MMP-2 and MMP-9 expression was markedly decreased in siPKC zeta-treated A549 cells, which exhibited a significantly decreased invasive capacity in the Transwell invasion assay (P<0.05). In conclusion, PKC zeta promoted lung adenocarcinoma invasion and metastasis, and its expression was associated with MMP-2 and MMP-9 expression. PKC zeta may be a potential target for gene therapy in lung adenocarcinoma.