NCAPG promotes the development of gastric adenocarcinoma and induces immune escape in mice
[Objective]To study the effect of clusterin Ⅰ complex subunit G(NCAPG)on the development of gastric adeno-carcinoma and immune escape related factors,we observed the changes of gastric adenocarcinoma AGS cells in vitro and in vivo after interfering with NCAPG,in order to provide new ideas for the treatment of gastric adenocarcinoma.[Method]Both nude mice and AGS cells were divided into 3 groups:control group,si-NC group and si-NCAPG group.CCK-8 was used to detect cell proliferation.The expression levels of clinical IL-2,IFN-γ,TNF-α and PD-L1 mRNA were detected by real-time quantitative PCR.The expression level of Ki-67 in tumor tissues was detected by immunohistochemistry.The effect of NCAPG on apoptosis of AGS cells was detected by flow-through technique.The expression levels of PI3KAKT proteins were detected by Western Blot.[Result]Compared with the control group and si-NC,The si-NCAPG group had the slowest tumor growth rate(466.56±15.02 vs 503.97±12.88 vs 203.78±10.22)and higher Bax/Bcl-2 ratio,Ki-67 expression decreased,IL-2,IFN-γ and TNF-α mRNA levels increased,and PD-L1 mRNA level decreased,phosphorylation of PI3K and AKT(P＜0.05).Compared with the control group and si-NC group,the cell proliferation was the lowest,the apoptosis rate was the highest,the mRNA levels of IL-2,IFN-γ and TNF-α were increased,the mRNA level of PD-L1 was decreased,and the phosphorylation levels of PI3 K and AKT protein were decreased in the si-NCAPG group(P＜0.05).[Conclusion]NCAPG promotes gastric adenocarcinoma and induces immune escape,and its mechanism of action may be related to the PI3K/AKT signaling pathway.
NETL
NSTL
万方数据
