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Light Preference Assay to Study Innate and Circadian Regulated Photobehavior in Drosophila Larvae
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Circadian regulator NR1D2 regulates glioblastoma cell proliferation and motility

Min Yu1, Wenjing Li1, Qianqian Wang1

  • 1State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China.

Oncogene
|May 19, 2018
PubMed

Insights

Nuclear receptor NR1D2 promotes glioblastoma (GBM) growth by regulating AXL and affecting cell motility. Targeting NR1D2 offers a potential therapeutic strategy for GBM.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Nuclear receptor NR1D2, known for regulating circadian rhythm, is increasingly found overexpressed in cancers.
  • Its specific roles and pathways in cancer, particularly glioblastoma (GBM), are not well understood.

Purpose of the Study:

  • To investigate the role of NR1D2 in glioblastoma (GBM).
  • To identify NR1D2 targets and pathways involved in GBM progression.

Main Methods:

  • NR1D2 expression analysis in GBM tissues and cell lines versus astrocytes.
  • Functional assays including cell proliferation, motility, and apoptosis after NR1D2 silencing.
  • RNA sequencing (RNA-seq) and Chromatin Immunoprecipitation (ChIP) assays.
  • Western blotting to assess protein levels and signaling pathways (PI3K/AKT, FAK, actin-related proteins).

Main Results:

  • NR1D2 is highly expressed in GBM but not in normal astrocytes.
  • NR1D2 silencing inhibits GBM cell proliferation and motility without affecting apoptosis.
  • AXL receptor tyrosine kinase identified as a direct transcriptional target of NR1D2.
  • NR1D2 regulates the PI3K/AKT pathway via AXL, promoting GBM cell proliferation, migration, and invasion.
  • NR1D2 knockdown impairs focal adhesion maturation and actin assembly, downregulating key proteins like p-FAK, p-Rac1/Cdc42, WAVE, and PFN2.
  • NR1D2 influences epithelial-to-mesenchymal transition (EMT) and cell motility through multiple targets beyond AXL.

Conclusions:

  • NR1D2 plays a significant role in promoting glioblastoma growth and progression.
  • NR1D2 targets, including AXL, mediate its effects on cell proliferation, migration, invasion, and motility.
  • NR1D2 represents a potential therapeutic target for glioblastoma treatment.

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