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NR2F6 regulates Temozolomide resistance in glioma via the E2F2-PARP1 pathway

Bo Wang1, Pengfei Xue2, Rongrong Li1

  • 1Joint Laboratory for Translational Medicine Research, Liaocheng People's Hospital, Liaocheng, 252000, Shandong Province, P.R. China.

Cancer Cell International
|October 22, 2025
PubMed
Abstract

Insights

Nuclear receptor NR2F6 promotes temozolomide (TMZ) resistance in glioma by upregulating E2F2 and PARP1. This mechanism enhances DNA repair, reducing treatment effectiveness and impacting patient prognosis in high-grade gliomas.

Area of Science:

  • Neuro-oncology
  • Molecular Biology
  • Genetics

Background:

  • Glioma is a common adult brain tumor, with temozolomide (TMZ) as a standard treatment.
  • Drug resistance to TMZ is a major challenge in malignant glioma therapy.
  • Understanding TMZ resistance mechanisms is crucial for improving patient outcomes.

Purpose of the Study:

  • To elucidate the role of NR2F6 in temozolomide (TMZ) resistance in glioma.
  • To investigate the molecular mechanisms underlying NR2F6-mediated TMZ resistance.

Main Methods:

  • Analysis of RNA sequencing data from TCGA and CGGA glioma cohorts.
  • Validation of NR2F6 expression in an in-house glioma patient cohort.
  • In vitro construction of TMZ-resistant glioma cell lines to study NR2F6 function.

Main Results:

  • NR2F6 expression is significantly upregulated in high-grade gliomas, correlating with poor prognosis.
  • NR2F6 is upregulated in TMZ-resistant cells, inducing resistance in glioma cells.
  • The E2F2-PARP1 axis mediates NR2F6's role in TMZ resistance.

Conclusions:

  • NR2F6, a nuclear transcription factor, upregulates E2F2 transcription.
  • Increased E2F2 expression leads to enhanced PARP1 expression.
  • This pathway promotes TMZ-induced DNA damage repair, decreasing glioma sensitivity to TMZ.

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