The Study Of The Effect VIP On PI3K/Akt Signal Pathways In Dendritic Cells And Its Contribution In Antigen Presentation Of Gastric Cancer

Background:Gastric cancer is the most common gastrointestinal malignancy, it seriouslyharm to the human health. After the body cells become cancerous, the body mainlydepend on acquired immune surveillance function to do the immune clearance andeliminate the cancerous cells. In this immune function, antigen-presenting cells play akey role. Dendritic cells are the most powerful antigen-presenting cells so far inwell-known antigen-presenting currently. On the other hand, cancer cells also secreteimmunosuppressive factors, such as gastrointestinal hormones VIP, leading toimmune disorders, and ultimately preserved itself. Some studies suggest, VIP isinvolved in regulating many organismic immune functions by influencing PI3K/Aktsignaling pathway, and PI3K/Akt signaling pathways have an important role indifferentiation, survival, secretion of cytokines and other aspects of DCs. Sopresumably, VIP could be involved in speaking and regulation of gastric cancerantigen presentation through influencing PI3K/Akt signaling pathway.Objective：To investigate the role of VIP on impacting PI3K/Akt signaling pathway inDendritic cells and its contribution in antigen presentation of gastric cancer.Methods：Through the incubation experiments using drug intervention and MKN45, weused two methods (RT-PCR and immunocytochemistry) to detect the expressionchanges of PI3K/Akt signaling pathway molecules (PI3K, Akt, p-Akt) and antigen-presenting related molecules (CD80, CD86, CD40, MHC-II) after using VIP orLY294002intervention and MKN45to incubate on DCs. Then, we analyzed the roleof VIP on impacting PI3K/Akt signaling pathway and its effects on DC antigen-presenting cells in gastric cancer. Results:1. With the maturation of Dendritic cells, the expression of antigen-presentingrelated molecules (CD80, CD86, CD40, MHC-II) gradually increased.2. VIP inhibited obviously the costimulatory molecules (CD80, CD86, CD40,MHC-II) expression of Dendritic cells through PI3K/Akt signal pathway. MKN45cells may make the inhibitory effect of VIP enhanced.3. MKN45cells may inhibited the costimulatory molecules (CD80, CD86, CD40,MHC-Ⅱ) expression of Dendritic cells through other signal pathways.Conclusions:The expression of costimulatory molecules (CD80, CD86, CD40, MHC-Ⅱ) inDendritic cells was related to PI3K/Akt signal pathway.VIP inhibited thecostimulatory molecules expression of Dendritic cells through PI3K/Akt signalpathway, which may be one reason of VIP has a inhibiting influence in the antigenpresentation of the gastric cancer.