Related Experiment Video

Updated: Jul 17, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

The p53/p21 DNA damage-signaling pathway is defective in most meningioma cells

Huda H Al-Khalaf1, Boleslaw Lach, Ayman Allam

  • 1Department of Biological and Medical Research, King Faisal Specialist Hospital and Research Center, MBC# 03-66, 3354, Riyadh 11211, KSA.

Journal of Neuro-Oncology
|January 25, 2007
PubMed

Insights

The p53/p21 signaling pathway is defective in most meningioma cells, and tumor suppressors p53, p21, and PTEN show varied expression, suggesting their crucial roles in meningioma development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Neuroscience

Background:

  • Meningiomas are the most common central nervous system tumors.
  • The molecular mechanisms driving meningioma development are not fully understood.

Purpose of the Study:

  • To investigate the expression and function of tumor suppressor proteins p53, p21, and PTEN in primary meningioma cells.
  • To assess the integrity of the p53/p21 signaling pathway in response to DNA damage.

Main Methods:

  • Immunoblotting was used to quantify protein levels of p53, p21, and PTEN.
  • Primary meningioma cells were exposed to UV and gamma radiation to study p53 and p21 induction.
  • The functionality of the p53/p21-dependent gamma-ray signaling pathway was evaluated.

Main Results:

  • The p53/p21-dependent gamma-ray signaling pathway was found to be defective in 62% of the analyzed meningioma cell samples.
  • Significant variations in the expression levels of tumor suppressors p21, p53, and PTEN were observed, with up to 40-fold differences.
  • Differential expression patterns suggest distinct roles for these proteins in meningioma pathogenesis.

Conclusions:

  • The p53/p21 signaling pathway and the PTEN protein are implicated in the development of benign meningiomas.
  • Defects in DNA damage response pathways may contribute to meningioma formation.
  • Aberrant expression of key tumor suppressors highlights their importance in meningioma biology.

More Related Videos

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice10:13

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

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 daughter...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...