In this research project, we have obtained the following findings. First, we have found that a histone deacetylase, HDAC2, which acts as a transcription regulator, suppresses primary cilia formation in pancreatic ductal adenocarcinoma (PDAC) cells. On the other hand, inhibition or depletion of HDAC6, which was previously reported to be required for cilia resorption, had no effect on the number of primary cilia. Second, we have found that ablation of HDAC2 decreases expression of Aurora A kinase, which induces disassembly of primary cilia, in PDAC cells, suggesting Aurora A is a downstream protein of HDAC2. Third, we have shown that oncogenic K-Ras and HDAC2 independently function in suppression of primary ciliogenesis in PDAC cells (under revision).