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Interleukin-13 initiates signal transduction through IL-13Rα2 in human glioma cell lines via AP-1 pathway

Wednesday, September 14, 2016 — Poster Session I

3:00 p.m. – 4:30 p.m.
FAES Terrace
FDA/CBER
CANCER-2

Authors

  • R Bhardwaj
  • A Suzuki
  • P Leland
  • BH Joshi
  • RK Puri

Abstract

Glioblastoma (GBM) is one of the most deadly and aggressive forms of brain cancer with a median survival of less than two years. Previously, we have demonstrated that Interleukin 13 (IL-13) receptor alpha-2 (α2) is overexpressed in approximately 78% of GBM samples. We have also shown that IL-13 receptors (IL-13R) can be targeted by IL-13-Pseudomonas exotoxin for cancer therapy in pre-clinical studies. Several clinical trials in GBM patients have also been completed. However, the regulation of the IL-13/IL-13R axis is not understood completely and it is not clear whether IL-13 receptors are functional in GBM. Herein, we have investigated whether IL-13 can mediate signaling through IL-13Rα2 in human glioma cell lines. By immunocytochemistry, we examined the activation of the AP-1 family of transcription factors (c-Jun, Jun-D, Jun-B, c-Fos and Fra-1) after treating U251, A172 & U87 (IL-13R+) and T98G (IL-13R-) cell lines with IL-13. We observed a differential up-regulation of c-Jun and Fra-1 in IL-13Rα2 positive glioma cell lines where the number of c-Jun and Fra-1 immune-positive cells were significantly higher than in IL-13R negative T98G cells. These studies show that IL-13 can signal through AP-1 in vitro. We are currently investigating IL-13 signaling in primary and metastatic brain cancer specimens to determine if AP-1 is activated in-vivo.

Category: Cancer Biology