Advanced glycation end products promote ChREBP expression and cell proliferation in liver cancer cells by increasing reactive oxygen species.
Impact factor: 1.552
Level of evidence: VI
Protocol: Real-time PCR, western blot.
Statistical Analysis: Student’s t-test, P<0.05 considered significant.
Study Type: In vitro.
Results: In human liver cancer cells (HepG2), AGE treatment increases the number of cells in the S-phase, decreases the percentage of cells undergoing apoptosis, and stimulates intracellular ROS production when compared to a control treatment. It was shown with fluorescent microscopy that treatment with the antioxidant, NAC (N-acetyl cysteine), along with AGE, decreased the amount of ROS species present in the cell. NAC also decreased the induction of carbohydrate responsive element-binding protein (ChREBP) expression.
Discussion: This study shows evidence of AGEs inducing proliferation of human liver cancer cells by increasing ROS and ChREBP expression. Findings from this study highlight the AGE-ROS-ChREBP pathway as a potential target for treatment of liver cancer in diabetic patients and can potentially explain increased liver cancer mortality in diabetic patients.
Chen H, Li Y, Zhu Y, et al. Advanced glycation end products promote ChREBP expression and cell proliferation in liver cancer cells by increasing reactive oxygen species [published correction appears in Medicine (Baltimore). 2017 Dec;96(50):e9318]. Medicine (Baltimore). 2017;96(33):e7456. doi:10.1097/MD.0000000000007456.
Advanced Glycation end Products and Receptor for Advanced End Products in AA amyloidosis
Impact Factor: 2.4
Level Of Evidence : IV
Sample Size: 55 autopsy specimens used from 25 patients were used
Study Type: Autopsy Study
Statistical Analysis: Chi Square analysis
Methods: There were 55 autopsy specimens that were taken from 25 patients that all had suffered from either AA amyloidosis, AL amyloidosis, and senile cardiovascular ATTR amyloidosis. Various organs were used from these patients including the liver, the spleen, the kidney, and the heart. All of these organs had some amount of amyloid that had occurred in them. The steps of this study had included inducing the AA amyloidosis in a mice population and then introducing AGE-KLH, glucose, bovine serum, human fibronectin and laminin on the AGE-modified proteins. Rabbits were used in order to make the polyclonal Anti-AGE antibodies, and statistical analysis were performed, after quantification with RT-PCR using a chi square test.
Results: Every specimen that came from a patient who had AA-amyloidosis had contained AGEs especially in the liver, kidney, and the spleen. In addition to diabetes, and cardiovascular complications, amyloidosis may be another complication of AGE.
Röcken C, Kientsch-Engel R, Mansfeld S, et al. Advanced glycation end products and receptor for advanced glycation end products in AA amyloidosis. Am J Pathol. 2003;162(4):1213-1220. doi:10.1016/S0002-9440(10)63917-X