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Celecoxib Suppresses NF-κB p65 (RelA) and TNFα Expression Signaling in Glioblastoma

Hina Ahsan1,2, Shaukat Iqbal Malik1, Fawad Ali Shah3

  • 1Department of Bioinformatics and Biosciences, Faculty of Health and Life Sciences, Capital University of Science and Technology (CUST), Islamabad 44000, Pakistan.

Journal of Clinical Medicine
|October 28, 2023
PubMed
Abstract

Insights

Celecoxib effectively reduced glioblastoma (GBM) cell growth by inhibiting nuclear factor kappa-B (NF-κB p65 (RelA)) and tumor necrosis factor-alpha (TNFα) expression. This combination therapy shows promise for treating aggressive GBM by dampening inflammatory pathways.

Area of Science:

  • Neuro-oncology
  • Molecular biology
  • Pharmacology

Background:

  • Glioblastoma (GBM) exhibits significant genetic heterogeneity and infiltrative growth, often relapsing after treatment.
  • Constitutive activation of nuclear factor kappa-B (NF-κB p65 (RelA)) and tumor necrosis factor-alpha (TNFα) signaling pathways is common in GBM, contributing to invasion and chemoresistance.
  • The precise anti-tumor mechanisms of NF-κB p65 (RelA) and TNFα in GBM remain incompletely understood.

Purpose of the Study:

  • To investigate the expression profiles of NF-κB p65 (RelA) and TNFα in GBM.
  • To evaluate the efficacy of celecoxib, in combination with temozolomide (TMZ), in inhibiting the growth of the human GBM cell line SF-767.
  • To elucidate the anti-proliferative and anti-invasive mechanisms of celecoxib in GBM.

Main Methods:

  • Genome-wide expression profiling and enrichment analysis were employed.
  • Quantitative expression analysis and immune infiltration assessments were conducted.
  • The Microculture Tetrazolium Test (MTT) proliferation assay was utilized to determine cell viability and proliferation rates.

Main Results:

  • Upregulation of NF-κB p65 (RelA) and TNFα was observed in GBM cells.
  • Celecoxib demonstrated a dose-dependent reduction in SF-767 cell viability and proliferation.
  • Celecoxib significantly decreased NF-κB p65 (RelA) and TNFα expression, mitigating invasive characteristics by inhibiting NF-κB-mediated inflammatory cascades.

Conclusions:

  • Celecoxib therapy can mitigate the invasive properties of GBM cell lines.
  • Combination therapy with celecoxib and temozolomide may reduce GBM aggressiveness.
  • Celecoxib shows potential in dampening transcriptional and enzymatic activities of GBM-associated inflammatory genes, including NF-κB p65 (RelA) and TNFα.
Keywords:
celecoxibgene expression genesglioblastomasurvival analysistemozolomidetumor necrosis factor

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