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BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt

Yu Liu1, Sen Li1, Ruoping Chen1

  • 1Department of Neurosurgery, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200000, China.

Open Life Sciences
|September 1, 2022
PubMed

Insights

BTBD10 is downregulated in glioma, acting as a tumor suppressor. Overexpressing BTBD10 inhibits glioblastoma growth, promotes apoptosis, and arrests the cell cycle by affecting cyclin D1 and Akt pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Glioma is a common primary brain tumor with a poor prognosis.
  • Understanding the molecular mechanisms underlying glioma development is crucial for therapeutic advancements.

Purpose of the Study:

  • To investigate the role of BTBD10 in glioma tumorigenesis.
  • To determine the correlation between BTBD10 expression and glioma pathological grade.

Main Methods:

  • Quantitative analysis of BTBD10 mRNA and protein in glioma tissues and normal brain tissues using RT-PCR and Western blot.
  • Functional assays in U251 glioblastoma cells overexpressing BTBD10, including MTT assay, flow cytometry, and Western blot analysis for cell proliferation, apoptosis, cell cycle, cyclin D1, and p-Akt.
  • Lentiviral vectors were used for gene delivery.

Main Results:

  • BTBD10 mRNA and protein levels were significantly reduced in glioma tissues compared to normal brain tissues.
  • BTBD10 expression levels were inversely correlated with glioma pathological grade.
  • Overexpression of BTBD10 in U251 cells led to reduced proliferation, G0/G1 phase arrest, increased apoptosis, and decreased cyclin D1 and p-Akt levels.

Conclusions:

  • BTBD10 acts as a tumor suppressor in human glioma.
  • BTBD10 downregulation is associated with glioma progression.
  • BTBD10 inhibits glioblastoma proliferation and induces apoptosis via the cyclin D1 and Akt signaling pathways.
Keywords:
AktBTBD10apoptosiscyclin D1gliomaproliferation

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