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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...
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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.
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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Updated: May 28, 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

Rethinking residual p53 function in HPV-positive cervical cancer cells.

Sannia Farrukh1, Nezka Kavcic1, Giulia Canarutto1

  • 1International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.

Journal of Virology
|May 27, 2026
PubMed
Summary
This summary is machine-generated.

Human papillomavirus (HPV) infection can lead to cervical cancer by affecting the p53 tumor suppressor. This study found that residual p53 in HPV-positive cells actually promotes tumor growth, challenging previous assumptions.

Keywords:
HPVcervical cancergain-of-functionp53

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Last Updated: May 28, 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

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

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Human papillomavirus (HPV)-driven cancers are globally prevalent.
  • High-risk HPV oncoproteins, particularly E6, counteract p53-mediated apoptosis and promote cell proliferation.
  • Residual p53 activity in HPV-positive cells suggests potential gain-of-function roles.

Purpose of the Study:

  • To investigate the role of residual p53 in HPV-positive cervical cancer cells.
  • To determine if residual p53 exhibits gain-of-function (GOF) growth-promoting activities.
  • To generate a p53-knockout (KO) HPV-positive cell line for experimental analysis.

Main Methods:

  • Utilized CRISPR-Cas9 ribonucleic protein complex to create a p53 KO HeLa cell line.
  • Performed transcriptomic analysis to identify gene expression changes.
  • Conducted immunoprecipitation assays to confirm p53 conformation and interactions.

Main Results:

  • p53 KO cells exhibited significantly reduced growth and metabolic activity.
  • Transcriptomic data revealed enrichment of wild-type p53 pathways, indicating GOF activities.
  • Immunoprecipitation confirmed the presence of GOF p53 in transformed cells.

Conclusions:

  • Residual p53 possesses tumor-promoting functions in HPV-positive cervical cancer cells.
  • HPV may subvert p53 function through alternative mechanisms beyond simple degradation.
  • The generated p53 KO model system facilitates further investigation into p53's functional mechanisms in HPV-driven cancers.