Related Experiment Video

Updated: Oct 15, 2025

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

9.7K

The p53 Protein Family in the Response of Tumor Cells to Ionizing Radiation: Problem Development

O A Kuchur1, D O Kuzmina1, M S Dukhinova1

  • 1ITMO University, Saint-Petersburg, 191002 Russia.

Acta Naturae
|October 28, 2021
PubMed

Insights

Tumor cells activate survival mechanisms against radiation therapy, reducing treatment effectiveness. This review examines how p53, p63, and p73 proteins influence tumor radioresistance through p53-dependent and independent pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Radiotherapy

Background:

  • Tumor cells develop resistance to radiation therapy through activated survival mechanisms.
  • The p53 protein family, including p53, p63, and p73, is crucial in regulating intracellular signaling and influencing tumor cell response to radiation.
  • Understanding these resistance mechanisms is vital for improving cancer treatment efficacy.

Purpose of the Study:

  • To review the p53-dependent mechanisms contributing to tumor radioresistance.
  • To analyze the p53-independent pathways involved in overcoming radiation resistance in cancer cells.
  • To provide insights into potential strategies for enhancing radiotherapy effectiveness.

Main Methods:

  • Literature review of studies on tumor cell survival mechanisms.
  • Analysis of the role of p53, p63, and p73 proteins in radioresistance.
  • Examination of both p53-dependent and p53-independent signaling pathways.

Main Results:

  • Ionizing radiation triggers survival pathways in tumor cells, leading to treatment resistance.
  • The p53 protein family plays a significant role in mediating tumor radioresistance.
  • Both p53-dependent and p53-independent mechanisms contribute to the ability of tumor cells to withstand radiation exposure.

Conclusions:

  • Targeting p53-dependent and p53-independent pathways may offer strategies to sensitize tumors to radiation.
  • Further research into these mechanisms can lead to more effective cancer radiotherapy.
  • Understanding tumor cell survival is key to overcoming therapeutic resistance.
Keywords:
cell deathmalignant tumorsp53 family proteinradiation therapyradioresistance

More Related Videos

Purification of Ubiquitinated p53 Proteins from Mammalian Cells10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

2.4K
Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins10:24

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

14.3K

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...
4.7K
DNA Damage can Stall the Cell Cycle02:37

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...
9.5K
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.
36.6K
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...
7.1K
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...
6.6K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
8.4K