Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
Cell Migration01:09

Cell Migration

Cell migration, the process by which cells move from one location to another, is essential for the proper development and viability of organisms throughout their life. When cells are not able to migrate properly to their ordained locations, various disorders may occur. For example, disruption in cell migration causes chronic inflammatory diseases such as arthritis.
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.
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Revisiting the grand challenges in oral cancers: advances in biomarkers and treatment strategies.

Frontiers in oral health·2026
Same author

Oncogenic p53 induces mitotic errors in lung cancer cells by recopying DNA replication forks conferring targetable proliferation advantage.

Cell death and differentiation·2026
Same author

Oncogenic p53 induces mitotic errors in lung cancer cells by recopying DNA replication forks conferring targetable proliferation advantage.

Research square·2025
Same author

A new drug target for NRAS(Q61) mutant-expressing cancers.

Nature reviews. Drug discovery·2025
Same author

Suppression of SIGMAR1 hinders oral cancer cell growth via modulation of mitochondrial Ca<sup>2+</sup> dynamics.

Molecular biology reports·2025
Same author

Silencing centromeres with age.

Nature reviews. Molecular cell biology·2025

Related Experiment Video

Updated: May 16, 2026

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

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

Published on: December 30, 2025

Mutant p53 in cell adhesion and motility.

W Andrew Yeudall1, Katharine H Wrighton, Sumitra Deb

  • 1Philips Institute of Oral & Craniofacial Molecular Biology, School of Dentistry, Virginia Commonwealth University, Richmond, VA, USA.

Methods in Molecular Biology (Clifton, N.J.)
|November 15, 2012
PubMed
Summary

Gain-of-function mutant p53 proteins promote cancer progression by enhancing cell migration and adhesion. Different mutant p53 alleles exhibit varying effects on migratory ability, influencing tumor development.

More Related Videos

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

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Related Experiment Videos

Last Updated: May 16, 2026

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

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

Published on: December 30, 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

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The p53 tumor suppressor gene is frequently mutated in human cancers.
  • Gain-of-function (GOF) p53 mutants can acquire new oncogenic functions beyond the loss of tumor suppression.

Purpose of the Study:

  • To investigate the pro-oncogenic properties of GOF p53 mutants.
  • To determine the impact of mutant p53 on cell migration, adhesion, and anchorage-independent growth.

Main Methods:

  • Stable expression of GOF p53 mutants in cancer cells (H1299) and fibroblasts (NIH3T3).
  • Cell migration assessed using wound-healing (scratch) and haptotactic (chamber) assays.
  • Cell adhesion evaluated through assays measuring attachment to extracellular matrix.
  • Anchorage-independent growth assessed via soft agar assays.

Main Results:

  • Cells expressing GOF p53 mutants exhibited significantly increased migration compared to controls.
  • Enhanced cell adhesion to the extracellular matrix was observed in cells with mutant p53.
  • Different p53 mutants displayed varying migratory potentials, indicating allele-specific effects.
  • Stable expression of a specific mutant p53 (H179L) enabled anchorage-independent growth in NIH3T3 fibroblasts.

Conclusions:

  • GOF mutant p53 proteins possess pro-oncogenic properties that drive cancer progression.
  • Mutant p53 enhances critical cellular processes like migration and adhesion.
  • The specific effects of mutant p53 on cell behavior can be allele-dependent.