Feedback circuitry between miR-218 repression and RTK activation in glioblastoma.

ABSTRACT: Receptor tyrosine kinase (RTK) signaling promotes the growth and progression of glioblastoma (GBM), a highly aggressive type of brain tumor. We previously reported that decreased miR-218 expression in GBM directly promotes RTK activity by increasing the expression of key RTKs and their signaling mediators, including the RTK epidermal growth factor receptor (EGFR), phospholipase C-γ1 (PLCγ1), and the kinases PIK3CA and ARAF. However, increased RTK signaling usually activates negative feedback mechanisms to maintain homeostasis. We found that decreased miR-218 expression in GBM cells also increased the expression of genes encoding additional upstream and downstream components of RTK signaling pathways, including the RTK platelet-derived growth factor receptor α (PDGFRα) and the kinases ribos

SUBMITTER: Mathew LK 

PROVIDER: S-EPMC4437515 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature