作者: Nikolina Radulovich , Nhu-An Pham , Dan Strumpf , Lisa Leung , Wing Xie
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摘要: The cyclin D1 (CCND1) and D3 (CCND3) are frequently co-overexpressed in pancreatic ductal adenocarcinoma (PDAC). Here we examine their differential roles PDAC. CCND1 CCND3 expression were selectively suppressed by shRNA PDAC cell lines with levels of equal (BxPC3), enhanced (HPAC) or (PANC1). Suppression proliferation was greater than downregulation. suppression led to a reduced level phosphorylated retinoblastoma protein (Ser795p-Rb/p110) resulted decreased A mRNA protein. global gene analysis identified deregulated genes D1- D3-cyclin siRNA-treated PANC1 cells. downregulated targets cells significantly enriched cycle associated processes (p < 0.005). In contrast, focal adhesion/actin cytoskeleton, MAPK NF B signaling appeared characterize the target interacting proteins Our results suggest that is primary driver cycle, cooperation integrates extracellular mitogenic signaling. We also present evidence plays role tumor migration. provide novel insights for common overexpression during duct carcinogenesis.