Related Experiment Video

Updated: Jun 29, 2025

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells
08:02

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells

Published on: September 23, 2021

2.6K

TCTP regulates genotoxic stress and tumorigenicity via intercellular vesicular signaling

Robert Amson1, Andrea Senff-Ribeiro1, Teele Karafin1

  • 1Institut Gustave Roussy (IGR), Unité Inserm U981, Bâtiment B2M, 114 rue Édouard-Vaillant, 94805, Villejuif, France.

EMBO Reports
|March 29, 2024
PubMed

Insights

Translationally controlled tumor protein (TCTP) is crucial for cancer cell communication via extracellular vesicles (EVs). Inhibiting TCTP reduces tumor growth and improves survival in mice, highlighting its role in oncogenic signaling.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Cancer Research

Background:

  • Extracellular vesicles (EVs) mediate intercellular signaling in cancer, but their regulatory mechanisms are poorly understood.
  • Translationally controlled tumor protein (TCTP) is found in EVs and may influence cancer progression.

Purpose of the Study:

  • To investigate the role of TCTP in genotoxic stress signaling and malignant transformation.
  • To elucidate the mechanisms by which TCTP regulates EV-mediated signaling in cancer.

Main Methods:

  • Generated a Tctp-inducible knockout mouse model (Tctp-/f-).
  • Utilized human breast cancer cells with TCTP knockdown.
  • Derived tumor cells from Trp53-/-;Tctp-/f- double mutant mice.
  • Administered sertraline to Trp53-/- mice.

Main Results:

  • TCTP is essential for genotoxic stress-induced apoptosis signaling via small EVs (sEVs).
  • TCTP knockdown impairs EV secretion and reduces sEV-dependent malignant growth in breast cancer cells.
  • Trp53-/-;Tctp-/f- mice exhibited significantly reduced tumorigenicity and prolonged survival.
  • Sertraline treatment increased survival in Trp53-/- mice.
  • TCTP binds DDX3, facilitating RNA and miRNA recruitment into sEVs.

Conclusions:

  • TCTP is a key regulator of sEV-mediated intercellular communication in apoptosis and tumorigenesis.
  • Targeting TCTP represents a potential therapeutic strategy for cancer treatment.
Keywords:
Bystander EffectSignalingSmall Extracellular Vesicles (sEVs)Tumor ReprogrammingTumor Reversion

More Related Videos

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells09:01

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

332
Gap Junctional Intercellular Communication: A Functional Biomarker to Assess Adverse Effects of Toxicants and Toxins, and Health Benefits of Natural Products05:27

Gap Junctional Intercellular Communication: A Functional Biomarker to Assess Adverse Effects of Toxicants and Toxins, and Health Benefits of Natural Products

Published on: December 25, 2016

15.0K

Related Concept Videos

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...
6.3K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.8K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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...
8.8K
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...
4.5K
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
1.3K
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...
7.4K