Fig. 6: Signalling alteration of IGF-1R networks in the absence and presence of the hsa-miR-12528. | Cell Death & Disease

Fig. 6: Signalling alteration of IGF-1R networks in the absence and presence of the hsa-miR-12528.

From: The novel hsa-miR-12528 regulates tumourigenesis and metastasis through hypo-phosphorylation of AKT cascade by targeting IGF-1R in human lung cancer

Fig. 6

The dynamic signalling graphics model based on the presence and absence of miR-12528. The upregulated IGF-1R in NSCLC mediates the interaction of ligands such as IGF-1. Upon internalization between the extracellular ligand and receptor, IGF-1R networks mediate the hyperphosphorylation of the Akt/mTOR, which subsequently leads to the development or progression of NSCLC. In the presence of miR-12528, blocking IGF-1R translation leads to a reduction of the interaction between IGF-1R and its ligand via the lack of the ligand-binding regions, and induces hypo-phosphorylation. Consequently, miR-12528 can negatively regulate NSCLC progression by modulating the cell cycle and apoptotic programmed cell death

Back to article page