
IndraLab
Statements
reach
"Herein, we observed a significant decrease expression level of total PI3K-p85, p-PI3K-p85, total Akt, p-Akt, GSK-3β and p-GSK-3β, as well as their downstream, β-catenin, c-Myc and cyclin D1 after treatment with Chr-A at different concentrations for 48 h in U251 and U87-MG cells, suggesting that Chr-A could downregulate PI3K-activated Akt followed by downregulation of GSK-3β, thus attenuating expression of β-catenin and downstream, c-Myc, cyclin D1, slug, MMP2 and MMP9 to inhibit proliferation and the EMT process of human glioblastoma cells."
reach
"Notably, inhibition of glycolysis effectively killed sensitive and resistant leukaemia cells and potently restored the sensitivity of MDR cells to the anticancer agent ADM. The AKT serine/threonine kinase (AKT)/mechanistic target of rapamycin (mTOR) signalling pathway, a crucial regulator of glycometabolic homeostasis, mediated over-activation and upregulation of c-Myc expression levels in K562 and ADM cells, which directly stimulated glucose consumption and enhanced glycolysis."
reach
"We found that inhibiting AKT with MK-2206 attenuated Sema3C-mediated stemness and reduced Gli1 and c-Myc expression, providing new evidence that Sema3C functions via the AKT/Gli1/c-Myc axis in HCC cells.In general, as a secreted protein, Sema3C needs to bind to receptors on the cell surface to perform specific functions."