IKBKE regulates angiogenesis by modulating VEGF expression and secretion in glioblastoma

As a noncanonical inflammatory kinase, IKBKE is frequently overexpressed and activated and has been identified as an oncogenic protein in glioblastoma. However, the potential function and underlying mechanism of IKBKE contributing to tumor angiogenesis remain elusive.

First, we analyzed the correlation between IKBKE and VEGF expression in glioma samples by immunohistochemistry (IHC). Second, HUVEC-related assays and Western blot were used to detect the regulatory effect of IKBKE on angiogenesis by modulating VEGF expression. Third, IKBKE depletion could alleviate the influence of VEGF expression on IHC of intracranial glioma model.

We demonstrate that depletion of IKBKE markedly inhibits tumor growth and angiogenesis in glioblastoma. Mechanistically, IKBKE induces VEGF expression and secretion by regulating AKT/FOXO3a in glioblastoma.

This study reveals that IKBKE is a novel oncogenic molecule that induces angiogenesis through the promotion of VEGF expression and highlights the potential of targeting IKBKE for glioblastoma therapy.