Related Experiment Video

Updated: May 25, 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

p53 inhibits angiogenesis by inducing the production of Arresten

Sarah Assadian1, Wissal El-Assaad, Xue Q D Wang

  • 1Goodman Cancer Research Center, Department of Biochemistry, McGill University, Montréal, Québec, Canada.

Cancer Research
|January 19, 2012
PubMed

Insights

The tumor suppressor p53 induces collagen IV expression and releases the anti-angiogenic factor Arresten. This process inhibits tumor growth by limiting angiogenesis, linking p53 to cancer suppression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • Collagen IV contains cryptic antiangiogenic domains released by extracellular matrix (ECM) proteolysis.
  • Arresten, a collagen-derived antiangiogenic factor (CDAF), is processed from α1 collagen IV.
  • The in vivo release of Arresten and its role in tumor suppressor pathways are largely unknown.

Purpose of the Study:

  • To investigate the conditions for Arresten release from collagen IV in vivo.
  • To determine if Arresten functions in tumor suppressor pathways.
  • To elucidate the mechanism by which p53 influences collagen IV and Arresten production.

Main Methods:

  • Analysis of COL4A1 transcriptional activation by p53 in human adenocarcinoma cells.
  • Identification of p53 binding sites on the COL4A1 gene.
  • Assessment of p53's effect on α(II) prolyl-hydroxylase and matrix metalloproteinase (MMP) activity.
  • In vivo studies of tumor growth inhibition and angiogenesis.
  • Immunostaining of Arresten and correlation with p53 status in prostate cancer.

Main Results:

  • p53 induces α1 collagen IV expression and Arresten release from ECM.
  • p53 directly activates COL4A1 transcription via an enhancer region.
  • p53 upregulates α(II) prolyl-hydroxylase, stabilizing α1 collagen IV and increasing Arresten release via MMPs.
  • Tumor cell production of α1 collagen IV and Arresten inhibits angiogenesis and limits tumor growth in vivo.
  • Arresten immunostaining correlates with p53 status in human prostate cancer.

Conclusions:

  • p53 links to the Arresten production pathway.
  • p53 inhibits angiogenesis through a novel mechanism involving collagen IV and Arresten.
  • This study reveals a new role for p53 in tumor suppression via anti-angiogenesis.

More Related Videos

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

Yeast As a Chassis for Developing Functional Assays to Study Human P5314:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

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.
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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...
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...