Related Experiment Video

Updated: Aug 16, 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

FGF1 inhibits p53-dependent apoptosis and cell cycle arrest via an intracrine pathway

Sylvina Bouleau1, Hélène Grimal, Vincent Rincheval

  • 1Laboratoire de Génétique et Biologie Cellulaire, Université de Versailles/Saint Quentin-en Yvelines, CNRS FRE 2445, France.

Oncogene
|August 11, 2005
PubMed

Insights

The p53 tumor suppressor pathway and the fibroblast growth factor 1 (FGF1) survival pathway interact to control cell fate. Intracellular FGF1 inhibits p53-dependent apoptosis and promotes cell proliferation, potentially impacting tumor progression.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The p53 protein is a critical tumor suppressor involved in apoptosis and cell cycle arrest.
  • Fibroblast Growth Factor 1 (FGF1) is implicated in cell survival and proliferation pathways.

Purpose of the Study:

  • To investigate the interplay between p53-induced apoptosis and the FGF1 survival pathway.
  • To elucidate the mechanisms by which FGF1 influences p53 activity.

Main Methods:

  • Analysis of gene expression in rat embryonic fibroblasts.
  • Investigation of protein-protein interactions and degradation pathways.
  • Assessment of p53 transactivation activity for target genes like BAX and p21.

Main Results:

  • p53 activation downregulates FGF1 expression, suggesting fgf1 is a repressed p53 target.
  • Intracellular FGF1 inhibits p53-dependent apoptosis and cell growth arrest via an intracrine mechanism.
  • FGF1 increases MDM2, accelerating p53 degradation and inhibiting p53-mediated BAX transactivation.

Conclusions:

  • The p53 and FGF1 pathways interact to determine cell fate, balancing proliferation and cell death.
  • Deregulation of these pathways can disrupt cellular homeostasis and contribute to tumor progression.
  • Intracellular FGF1 acts as a negative regulator of p53 tumor suppressor functions.

More Related Videos

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells13:38

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells

Published on: January 18, 2017

Related Concept Videos

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.
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...
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...
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...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...