Insulin-mediated signaling promotes proliferation and survival of glioblastoma through Akt activation.

ABSTRACT:

Background

Metabolic complications such as obesity, hyperglycemia, and type 2 diabetes are associated with poor outcomes in patients with glioblastoma. To control peritumoral edema, use of chronic high-dose steroids in glioblastoma patients is common, which can result in de novo diabetic symptoms. These metabolic complications may affect tumors via profound mechanisms, including activation of insulin receptor (InsR) and the related insulin-like growth factor 1 receptor (IGF1R) in malignant cells.

Methods

In the present study, we assessed expression of InsR in glioblastoma surgical specimens and glioblastoma response to insulin at physiologically relevant concentrations. We further determined whether genetic or pharmacological targeting of InsR affected oncogenic functions of

SUBMITTER: Gong Y 

PROVIDER: S-EPMC4677408 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature