TITLE:
The Activity of AQP9 Is Mediated MAPK in Arsenic-Treated Mouse Model of Hepatocellular Carcinoma
AUTHORS:
Qianqian Wang, Ping Wang, Xiaozhen Wang, Xiaowen Wang, Zeyan Zhang, Fuzhi Lian, Rong Zhen, Yifei Cao
KEYWORDS:
AQP9, Phosphorylation, P38, JNK, Arsenic
JOURNAL NAME:
Advances in Bioscience and Biotechnology,
Vol.13 No.12,
December
29,
2022
ABSTRACT: Background: Arsenic
metabolism is primarily undergoing in hepatocytes, but the underlying
mechanisms are to be defined. It is essential to study the response of
aquaporin AQP9, protein kinase p38, and JNK with the stimulation of arsenic in
mouse models of hepatocellular carcinoma. Methods: Mouse model of
hepatocellular carcinoma (HCC) was induced with H22 cells injected
subcutaneously on the lateral side of each right axilla in C57BL/6 mice. Then,
western blotting and co-immunoprecipitation were used to detect the protein
expression and phosphorylation of molecules AQP9, p38 and JNK in mouse models
of hepatocellular carcinoma, respectively. The hepatocellular distribution of
AQP9 was examined by the immunofluorescent method. Results: In both wild
mice and a mouse model of liver tumor, there was no significant difference in
the expressions of AQP9, protein kinase p38, and JNK after arsenic treatment,
but the phosphorylation expression levels of the three were significantly
increased to varying degrees, and the tumor model Compared with the wild-type
group, the expression increased. Laser confocal experiments showed that in
HepG2 cells, phosphorylated AQP9 was mainly distributed on the cell membrane
under the stimulation of arsenic. Conclusion: Arsenic stimulation can
increase the phosphorylation of AQP9, p38, and JNK in both wild-type C57 mice
and liver tumor mice models. Arsenic stimulation facilitates
phosphorylated-AQP9 predominantly distributed on the cell membrane of hepatoma
cells HepG2.