Recent data implicate AQP3 as an important determinant in epidermal proliferation and skin tumorigenesis, in which AQP3-knockout mice are resistant to tumor formation by a mechanism that may involve reduced cell glycerol content and ATP energy for biosynthesis.
These observations identify AQP3 and CD24 as biomarkers for carcinogenesis of GIM, and may provide a precise strategy for screening at-risk candidates with GIM.
In the present study, we proved the carcinogenesis roles of aquaporin 3 (AQP3) in hepatocellular carcinoma (HCC) and demonstrated that AQP3 promotes the stem cell-like properties of hepatoma cells by regulating CD133 expression.
Over-expression of AQP1, AQP3 and AQP5 is clearly associated with carcinogenesis, metastasis, reduced survival rate, lymph node metastasis, poorer prognosis, and cellular migration.
Here we report that H. pylori infection-mediated carcinogenesis may be mechanistically depended on the upregulation of AQP3 expression via reactive oxygen species (ROS) pathway activation in the stomach.
35 PDA samples in different stages of differentiation and locations were analyzed by immunohistochemistry for expression of AQP5, AQP3 and several markers of cell proliferation and tumorigenesis.