Downregulation of L1CAM inhibits proliferation, invasion and arrests cell cycle progression in pancreatic cancer cells in vitro

作者：Qiwen Ben, Wei An, Jian Fei, Maojin Xu, Guixiang Li, Zhao‐Shen Li, Yaozong Yuan · 发表于：Experimental and Therapeutic Medicine · 年份：2014 · DOI：10.3892/etm.2014.1519 · 被引用次数：36 · 研究领域：Pancreatic function and diabetes、Phagocytosis and Immune Regulation、Pancreatic and Hepatic Oncology Research

The aim of the present study was to establish the effect of silencing L1 cell adhesion molecule (L1CAM) on the proliferation, invasion, cell cycle progression and apoptosis of pancreatic cancer cells, and to determine the potential molecular mechanisms that are involved. The human Capan-2 pancreatic cancer cell line was infected with lentivirus-mediated short hairpin RNA (shRNA) to target L1CAM. Cell proliferation and invasion were analyzed using cell counting kit-8 and Transwell assays, respectively, and cell cycle progression and apoptosis were analyzed using flow cytometry. L1CAM protein expression in Capan-2 cells decreased following shRNA-L1CAM infection. Furthermore, knockdown of L1CAM significantly inhibited cell proliferation and reduced the number of invasive cells, while increasing the percentage of cells in the G0/G1 phase (P<0.05). However, the effect on apoptosis was not identified to be statistically significant. In addition, L1CAM silencing may induce activation of p38/extracellular signal regulated kinase 1/2. Downregulation of L1CAM may inhibit proliferation, invasion and arrests cell cycle progression in pancreatic cancer via p38/ERK1/2 signal pathway, and therefore, L1CAM may serve as a potential target for gene therapy in pancreatic cancer.