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Down-Regulation of CEND1 Expression Contributes to The Progression and Temozolomide Resistance of Glioma

Zhou Houjun1, Bai Peng1

  • 1Neurosurgery Department 2, The Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.

Cell Journal
|May 21, 2023
PubMed
Abstract

Insights

Cell cycle exit and neuronal differentiation 1 (CEND1) is downregulated in glioma, inhibiting tumor growth, migration, and temozolomide (TMZ) resistance by suppressing the NF-κB pathway.

Area of Science:

  • Neuro-oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Glioma is a primary brain tumor with poor prognosis.
  • Cell cycle exit and neuronal differentiation 1 (CEND1) is a key regulator of cell fate.
  • The role of CEND1 in glioma progression and treatment resistance remains unclear.

Purpose of the Study:

  • To investigate CEND1 expression in glioma.
  • To determine the impact of CEND1 on glioma cell proliferation, migration, invasion, and temozolomide (TMZ) resistance.
  • To elucidate the molecular mechanisms underlying CEND1's function in glioma.

Main Methods:

  • Bioinformatic analysis of CEND1 expression in glioma tissues and patient survival.
  • Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry for CEND1 detection.
  • Cell viability assays (CCK-8), proliferation assays (BrdU), migration assays (wound healing), and invasion assays (Transwell).
  • Bioinformatic pathway analysis (KEGG, GO, GSEA) and Western blot for NF-κB signaling pathway assessment.

Main Results:

  • CEND1 expression is significantly reduced in glioma tissues and cells, correlating with shorter patient survival.
  • CEND1 knockdown enhances glioma cell proliferation, migration, and invasion, and increases resistance to TMZ.
  • CEND1 overexpression exhibits opposite effects, suppressing tumor growth and chemosensitivity.
  • CEND1 co-expression analysis revealed enrichment in the NF-κB pathway; CEND1 modulates NF-κB p65 phosphorylation.

Conclusions:

  • CEND1 functions as a tumor suppressor in glioma.
  • CEND1 inhibits glioma cell proliferation, migration, invasion, and TMZ resistance.
  • CEND1 exerts its inhibitory effects by suppressing the NF-κB signaling pathway.
Keywords:
CEND1GliomaProliferationTemozolomide

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