Related Experiment Video

Updated: Jan 19, 2026

Translational Orthotopic Models of Glioblastoma Multiforme
07:37

Translational Orthotopic Models of Glioblastoma Multiforme

Published on: February 17, 2023

3.6K

MTBP regulates cell survival and therapeutic sensitivity in TP53 wildtype glioblastomas

Yifu Song1, Li Zhang1, Yang Jiang1,2

  • 1Department of Neurosurgery, The First Hospital of China Medical University, Shenyang 110001, China.

Theranostics
|September 20, 2019
PubMed

Insights

Myeloid-associated regulatory factor (MTBP) promotes glioblastoma (GBM) survival and treatment resistance by stabilizing p53 via MDM2. Targeting MTBP may improve outcomes for patients with TP53-wildtype GBM.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Glioblastoma (GBM) is an aggressive brain tumor characterized by high proliferation and resistance to standard therapies.
  • TP53 tumor suppressor gene mutations or functional loss are common in GBM, often mediated by the p53 signaling axis.
  • Myeloid-associated regulatory factor (MTBP) influences MDM2 and p53 activity, prompting investigation into its role in TP53-wildtype GBM.

Purpose of the Study:

  • To investigate the role of MTBP in the biological behavior of TP53-wildtype GBM.
  • To determine the impact of MTBP modulation on GBM cell viability, apoptosis, clonogenicity, and response to therapy.
  • To elucidate the regulatory mechanisms of MTBP and its interaction with the p53-MDM2 pathway.

Main Methods:

  • Analysis of MTBP expression in TCGA and REMBRANDT datasets.
  • In vitro and in vivo studies involving MTBP knockdown or overexpression in TP53-wildtype GBM cells and glioma stem cells (GSCs).
  • Assessment of cell viability, apoptosis, clonogenicity, and response to radiation and temozolomide (TMZ) treatment.

Main Results:

  • MTBP upregulation correlated with the Classical molecular subtype and predicted poor GBM patient survival.
  • MTBP positively associated with MDM2 and negatively with p53 protein levels in TP53wt GBM cells.
  • MTBP knockdown induced apoptosis and reduced clonogenicity, while overexpression enhanced tumorigenicity; MTBP silencing sensitized GBM cells to radio-chemotherapy.

Conclusions:

  • MTBP promotes glioblastoma cell survival and resistance to therapy by regulating p53 stability through MDM2.
  • MTBP is transcriptionally regulated by c-myc, forming a positive feedback loop.
  • Targeting MTBP presents a potential therapeutic strategy to improve survival rates in TP53-wildtype GBM patients.
Keywords:
GliomaMDM2MTBPapoptosisp53

More Related Videos

The Clinical Application of Tumor Treating Fields Therapy in Glioblastoma08:00

The Clinical Application of Tumor Treating Fields Therapy in Glioblastoma

Published on: April 16, 2019

19.1K
Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma10:58

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Published on: February 22, 2015

13.4K

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.6K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.4K