NVS-ZP7-4 inhibits hepatocellular carcinoma tumorigenesis and promotes apoptosis via PI3K/AKT signaling.

NVS-ZP7-4 was identified as a novel chemical reagent targeting the zinc input protein ZIP7, which accounts for the zinc surge from the apparatus to the cytoplasm. Since zinc dysregulation is related to multiple diseases, in this study, we aimed to identify the anti-tumor effects of NVS-ZP7-4 and explore the molecular mechanisms of NVS-ZP7-4 in hepatocellular carcinoma (HCC) progression. We found that NVS-ZP7-4 inhibited cell viability, caused cell cycle arrest, induced apoptosis, and inhibited the proliferation, migration, and invasion of HCCLM3 and Huh7 cells. We further investigated the inhibited activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway was involved in the antitumor effect of NVS-ZP7-4 in HCC. Furthermore, NVS-ZP7-4 inhibited HCC tumor growth in vivo. The present study demonstrated that NVS-ZP7-4 is a promising therapeutic target for HCC by regulating PI3K/AKT signaling.

Desmoglein 3 contributes to tumorigenicity of pancreatic ductal adenocarcinoma through activating Src-FAK signaling.

Desmogleins (DSGs), with the ability to link adjacent cells, have been shown to participate in the development of malignancy. DSG3 was up-regulated in various cancers, including lung, head and neck, and esophagus squamous cell carcinoma, which contributed to the tumor progression. The role of DSG3 in pancreatic ductal adenocarcinoma (PDAC) still remains elusive. Here, the expression of DSG3 was found to be enhanced in pancreatic cancer cell lines in vitro. Functional assays showed that shRNA-mediated knockdown of DSG3 decreased cell viability of pancreatic cancer cells and retarded the cell proliferation, migration and invasion. However, pcDNA-mediated over-expression of DSG3 exhibited reversed effect on pancreatic cancer cell progression. In addition, the in vivo assay demonstrated that transfection of shDSG3 lentiviruses into pancreatic cancer cells repressed the tumorigenicity of PDAC after the cancer cells were transplanted into mice subcutaneously. Elevated DSG3 expression promoted the phosphorylation of Src (p-Src), focal adhesion kinase (p-FAK) and AKT (p-AKT) in vitro, while silence of DSG3 reduced the expression of p-Src, p-FAK and p-AKT both in vitro and in vivo. In conclusion, DSG3, as an oncogene, contributed to the tumorigenicity of PDAC through activating Src-FAK signaling.

The serum carbohydrate antigen 125 and carcinoembryonic antigen comparsion for the han and uyghur patients of terminal gallbladder cancer in xinjiang uygur autonomous region / 中国基层医药

Objective To compare the differences on the serum carbohydrate antigen 125 and carcinoembryonic antigen for the Han and Uyghur patients of terminal gallbladder cancer in Xinjiang Uygur Autonomous Region.Methods 80 cases of patients with primary advanced gallbladder,including 40 cases of Uighur,Han 40 cases,The cholecystitis patients randomly selected from the same period of hospitalization of 60 cases as the control group.Including 34 cases of Uighur and Han 26 cases,Levels of serum CA125,CEA were detected.Results The gallbladder group of Han,Uygur patients and the control group with ethnic patients CA125,CEA level differences were statistically significant(t =27.01,28.06,10.68,11.25,all P ＜ 0.05) ; CA125,CEA level differences between the two groups within the Han,Uygur patients were not statistically significant(t =0.47,0.34,0.1 l,1.23,all P ＞ 0.05) ; Han,Uygur patients with Stage V of gallbladder cancer stage Ⅳ with ethnic patients with CA125,CEA level differences were statistically significant (t =26.92,25.01,16.58,14.54,all P ＜ 0.05) ; CA125,CEA levels between the Han,Uygur gallbladder patients with stage Ⅳ and Ⅴ patients,the differences were not statistically significant (t =1.13,0.11,0.38,0.07,all P ＞ 0.05).Conclusion Xinjiang region of Han and Uygur advanced gallbladder serum CA125,CEA level differences in patients with advanced gallbladder CA125,CEA tests can help diagnose cases.