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...
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...
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...
Repressible Operon: trp Operon01:21

Repressible Operon: trp Operon

The trp operon in Escherichia coli exemplifies a repressible operon. It regulates the synthesis of tryptophan through repressor-mediated transcriptional control and attenuation. This dual regulatory mechanism ensures tryptophan biosynthesis occurs only when needed, conserving cellular resources.Structure of the trp OperonThe trp operon consists of five structural genes (trpE, trpD, trpC, trpB, and trpA) that encode enzymes for tryptophan biosynthesis. These genes are transcribed as a single...

You might also read

Related Articles

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

Sort by
Same author

Prevalence of homologous recombination repair genes alterations in metastatic castration-resistant prostate cancer, a multicentric study.

The French journal of urology·2026
Same author

Technical recommendations from a large-scale French Delphi consensus: A step toward European harmonization of ctDNA analysis.

European journal of cancer (Oxford, England : 1990)·2026
Same author

Deciphering the Role of Cancer Stem Cells in Breast Cancer Brain Colonization Using a Novel Patient-Derived Model.

Advanced healthcare materials·2026
Same author

FAK signaling pathways are modulated by HSPB8 and BAG3 in breast cancer.

Cell communication and signaling : CCS·2026
Same author

SH3BP5L triggers the RAB11A-regulated integrin recycling network implicated in breast cancer metastasis.

The Journal of clinical investigation·2026
Same author

Correction: Intraductal papilloma of the breast: low risk, but handle with care.

La Radiologia medica·2025
Same journal

Generalizable AI predicts immunotherapy outcomes across cancers and treatments.

Nature medicine·2026
Same journal

Immune aging biomarkers for clinical trials.

Nature medicine·2026
Same journal

Lassa fever countermeasures gather pace.

Nature medicine·2026
Same journal

Why high scores do not mean application readiness for health AI.

Nature medicine·2026
Same journal

Polypill for heart failure with reduced ejection fraction: the POLY-HF randomized trial.

Nature medicine·2026
Same journal

Biological aging might help to explain the rising risk of early-onset cancer.

Nature medicine·2026
See all related articles

Related Experiment Video

Updated: May 26, 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

Reciprocal repression between P53 and TCTP.

Robert Amson1, Salvatore Pece, Alexandra Lespagnol

  • 1Centre National de la Recherche Scientifique-Unité Mixte de Recherche 8113, Laboratoire de Biotechnologie et Pharmacologie génétique Appliquée, École Normale Supérieure, Cachan, France.

Nature Medicine
|December 14, 2011
PubMed
Summary
This summary is machine-generated.

Translationally controlled tumor protein (TCTP) promotes cancer cell survival by degrading P53. Inhibiting TCTP restores P53 levels, sensitizes tumors to apoptosis, and may offer new cancer treatment strategies.

More Related Videos

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

Establishment of Proliferative Tetraploid Cells from Nontransformed Human Fibroblasts
10:04

Establishment of Proliferative Tetraploid Cells from Nontransformed Human Fibroblasts

Published on: January 8, 2017

Related Experiment Videos

Last Updated: May 26, 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

Establishment of Proliferative Tetraploid Cells from Nontransformed Human Fibroblasts
10:04

Establishment of Proliferative Tetraploid Cells from Nontransformed Human Fibroblasts

Published on: January 8, 2017

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Translationally controlled tumor protein (TCTP) is implicated in cancer progression.
  • The tumor suppressor P53 plays a critical role in apoptosis and tumor suppression.
  • A regulatory relationship between TCTP and P53 has not been previously defined.

Purpose of the Study:

  • To elucidate the regulatory interaction between TCTP and P53.
  • To investigate the role of this interaction in cancer cell biology and prognosis.
  • To explore potential therapeutic strategies targeting the TCTP-P53 axis.

Main Methods:

  • Investigated the interaction between TCTP and P53 using biochemical assays.
  • Utilized Tctp haploinsufficient mouse models to study P53-dependent apoptosis.
  • Analyzed TCTP and P53 expression in human breast cancer samples.
  • Assessed the effect of Tctp knockdown in cancer cells.
  • Examined the impact of pharmacological compounds on the TCTP-P53 pathway.

Main Results:

  • Identified a negative feedback loop where TCTP promotes P53 degradation via the MDM2 complex.
  • P53 was found to directly repress TCTP transcription.
  • High TCTP levels in breast cancer correlate with aggressive G3 tumors and poor prognosis.
  • Tctp knockdown increased P53 expression and reduced stem-like cancer cells.
  • Sertraline and thioridazine were shown to increase P53 levels by targeting TCTP.

Conclusions:

  • Established a novel regulatory circuit between TCTP and P53, impacting apoptosis and tumor suppression.
  • TCTP's role in promoting P53 degradation highlights its significance in aggressive cancers.
  • Targeting TCTP offers a potential therapeutic avenue for enhancing P53 function and treating cancer.