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Protein kinase D (PKD) 1 influences cell migration by mediating bothtrans-Golgi vesicle fission and integrin recycling to the cell surface. Using restriction landmark genomic scanning methods, we found that the promoter region ofPKD1was aberrantly methylated in gastric cancer cell lines. Silencing ofPKD1expression was detected in 72.7% of gastric cancer cell lines examined, and the silencing was associated with CpG hypermethylation in the promoter region ofPKD1. Treatment with 5-aza-2′-deoxycytidine and trichostatin A partially reversedPKD1methylation and restored gene expression inPKD1-silenced cell lines. Real-time reverse transcription–polymerase chain reaction analysis of 96 paired clinical primary gastric cancer samples revealed that 59% of the analyzed tumors had a &gt;2-fold decrease inPKD1expression compared with each normal-appearing tissue and that this downregulation ofPKD1expression was significantly correlated with increased methylation. We also observed a gradual increase in the level of promoter methylation ofPKD1in aging, normal-appearing mucosal tissues, suggesting thatPKD1methylation may be one of the earliest events that predispose an individual to gastric cancer. PKD1 expression was required for directional migration of gastric cancer cells. Furthermore, knock down of PKD1 by RNA interference promoted the invasiveness of cell lines that expressed PKD1 at relatively high levels. Based on these results, we propose thatPKD1is frequently silenced by epigenetic regulation, which plays a role in cell migration and metastasis in gastric cancer.

Epigenetic inactivation of protein kinase D1 in gastric cancer and its role in gastric cancer cell migration and invasion