Expression of Nuclear Factor-κB, Tumor Necrosis Factor Receptor Type 1, and c-Myc in Human Astrocytomas

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  • HAYASHI Shuji
    Department of Neurosurgery, Fukuoka University School of Medicine
  • YAMAMOTO Masaaki
    Department of Neurosurgery, Fukuoka University School of Medicine Molecular Oncology Center, Fukuoka University School of Medicine
  • UENO Yushi
    Department of Neurosurgery, Fukuoka University School of Medicine
  • IKEDA Kohichi
    Department of Neurosurgery, Fukuoka University School of Medicine
  • OHSHIMA Koichi
    Department of Pathology, Fukuoka University School of Medicine
  • SOMA Gen-Ichiro
    Institute for Health Sciences, Tokushima Bunri University
  • FUKUSHIMA Takeo
    Department of Neurosurgery, Fukuoka University School of Medicine

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  • Expression of Nuclear Factor-κB, Tumor Necrosis Factor Receptor Type 1, and c-Myc in Human Astrocytomas

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Tumor necrosis factor receptor type 1 (TNFR1) and c-Myc are important in signal transduction in tumor necrosis factor-α (TNF-α)-induced cytotoxicity, whereas activation of nuclear factor-κB (NF-κB) protects against TNF-α-induced apoptosis. This study investigated the expression of NF-κB, TNFR1, and c-Myc in human astrocytoma tissues by reverse transcriptase-polymerase chain reaction (PCR) and immunohistochemical analysis. TNFR1 messenger ribonucleic acid (mRNA) and c-Myc mRNA were frequently expressed in malignant astrocytomas, especially in glioblastomas, compared with low-grade astrocytomas by PCR analysis. TNFR1 and c-Myc mRNAs were barely detectable in normal brain tissues. NF-κB p50 and p65 subunit mRNAs were detected in various grades of astrocytomas, with frequent expression in malignant astrocytomas. The presence of activated NF-κB was confirmed by nuclear localization in neoplastic astrocytes as determined by immunohistochemistry. Both p50 and p65 subunits were inhomogeneously expressed in neoplastic astrocytes of glioblastoma, but only in a few scattered tumor cells in low-grade astrocytoma, and almost undetectable in normal brain tissues. These results indicate that TNFR1 and c-Myc are overexpressed in malignant astrocytomas, and this may increase the cellular sensitivity to the cytotoxic action of TNF-α. NF-κB p50 and p65 were simultaneously induced and activated in malignant astrocytomas. Our results suggest that the constitutive activation of NF-κB subunits in malignant astrocytoma, especially in glioblastoma, could be associated with the resistance to TNF-α immunotherapy, and indicates new therapeutic strategies for malignant astrocytomas.<br>

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