| Objective: To investigate cholecystokinin-A receptor (CCK-AR) expression in human pancreatic carcinoma cell line Panc-1,explore the growth invasion change and possible mechanism by cholecystokinin-8S (CCK-8S) and CCK-AR antagonist Lorglumide in pancreatic carcinoma in vitro. Methods: ①. CCK-AR expression in Panc-1 cell was detected by RT-PCR. ②. CCK-8S and Lorglumide were cultured seperatively with Panc-1 cell. Cell growth change were examined by MTT. Flow cytometery(FCM) shew the cell cycle change. Apoptosis rate change and Caspase-3 expression were assessed through TUNEL and cell immunohistochemistry ③. Cell invasion ability was assessed by Invasion Assay. Wesem Blot and cell immunohistochemistry shew the change of MMP-2 expression. Results: ①. CCK-AR was expressed in Panc-1 cell. ②. CCK-8S promoted cell proliferation, this effect was increased with a dose and time dependent manner. CCK-8S increased the ratio in S stage of cell cycle , apoptosis rate and Caspase-3 expression was little. While Lorglumide inhibited the cell growth, mainly retarded in G1 cell cycle. Apoptosis rate and Caspase-3 expression increased highly. ③. CCK-8S promoted the cell invasion ability,this effect was increased with a dose dependent manner .Also CCK-8S promoted MMP-2 expression while Lorglumide has the contrary effect. Conclusions: With the "CCK—CCK-AR" pathway ,CCK-8S promoted Panc-1 cell growth and invasion though down-regulation of Caspase-3 and up-regulation of MMP-2 while Lorglumide inhibited this signal transduction effect.
|
PDF Full Text Request