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  1. Home
  2. Bptf Promotes Glioma Development Through Usp34-mediated De-ubiquitination Of Foxc1.
  1. Home
  2. Bptf Promotes Glioma Development Through Usp34-mediated De-ubiquitination Of Foxc1.

Related Experiment Video

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
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Published on: August 25, 2021

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BPTF promotes glioma development through USP34-mediated de-ubiquitination of FOXC1.

Yanling Pan1, Feng Yuan1, Zhiren Lin1

  • 1Department of Radiotherapy, Haikou Affiliated Hospital of Central South University Xiangya School of Medicine, Haikou, Hainan Province, PR China.

Histology and Histopathology
|April 30, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Brain cancer growth is driven by BPTF, which impacts FOXC1 stability. Targeting the BPTF/FOXC1 pathway may inhibit glioma development and improve patient outcomes.

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Investigating Protein-protein Interactions in Live Cells Using Bioluminescence Resonance Energy Transfer

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Area of Science:

  • Molecular Oncology
  • Cancer Biology
  • Neuro-oncology

Background:

  • Glioma, the most common malignant brain tumor, requires understanding its molecular drivers for clinical advancement.
  • Previous research identified Bromodomain PHD Finger Transcription Factor (BPTF) as a promoter of glioma malignancy and a predictor of poor prognosis.

Purpose of the Study:

  • To elucidate the downstream regulatory mechanisms of BPTF in glioma development.
  • To investigate the role of Forkhead Box C1 (FOXC1) in BPTF-mediated glioma progression.
  • To explore the potential of the BPTF/FOXC1 axis as a therapeutic target.

Main Methods:

  • Protein expression analysis using Western blot and immunohistochemistry.
  • Cellular assays (CCK8, flow cytometry, scratch, Transwell) to assess proliferation, apoptosis, and migration.
  • Biochemical assays (immunoprecipitation, Western blot) to determine protein interactions and ubiquitination status.
  • Main Results:

    • BPTF knockdown inhibited glioma cell malignant behaviors, correlating with decreased FOXC1 expression.
    • FOXC1 was upregulated in glioma tissues, associated with advanced tumor stage and poorer prognosis.
    • BPTF regulates FOXC1 stability via USP34-mediated de-ubiquitylation, impacting glioma progression.

    Conclusions:

    • The BPTF/FOXC1 signaling axis is a critical driver of glioma development.
    • Targeting the BPTF/FOXC1 pathway presents a potential therapeutic strategy for glioma inhibition.