Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The invasive nature of glioblastoma (GBM) is one important reason for treatment failure. GBM stem/progenitor cells retain the migratory ability of normal neural stem/progenitor cells and infiltrate the brain parenchyma. Here, we identify Rai (ShcC/N-Shc), a member of the family of Shc-like adaptor proteins, as a new regulator of migration of normal and cancer stem/progenitor cells. Rai is expressed in neurogenic areas of the brain and its knockdown impairs progenitor migration to the olfactory bulb. Its expression is retained in GBM stem/progenitor cells where it exerts the same promigratory activity. Rai silencing in cancer stem/progenitor cells isolated from different patients causes significant decrease in cell migration and invasion, both in vitro and in vivo, providing survival benefit. Rai depletion is associated with alteration of multiple-signaling pathways, yet it always leads to reduced expression of proinvasive genes.
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PMID:Rai is a new regulator of neural progenitor migration and glioblastoma invasion. 2231 6

Shc3 protein levels are high in human glioblastoma but they decrease in vitro. We found that SHC3 mRNA and protein increased when glioblastoma cells grew as multicellular tumor spheroid (MTS). Shc3 expression was also induced in adherent cultures by increasing cell density. Among the Shc family members, only Shc2 and Shc3 increased with cell density. Shc3 and focal adhesion kinase (Fak) interact as shown by co-immunoprecipitation. Inhibition of Fak activation reduced Shc3 increase and MTS formation and changed Shc3 phosphorylation pattern. Our results suggest that in gliomas cell density modulates Shc3 protein levels and its activity, at least in part, through Fak activation.
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PMID:Cell density modulates SHC3 expression and survival of human glioblastoma cells through Fak activation. 2506 68