Related Experiment Video

Updated: Jun 1, 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

Wild-type p53 attenuates cancer cell motility by inducing growth differentiation factor-15 expression

Jung-Chien Cheng1, Hsun-Ming Chang, Peter C K Leung

  • 1Department of Obstetrics and Gynecology, Child and Family Research Institute, University of British Columbia, 4490 Oak Street, Vancouver, British Columbia, Canada, V6H 3V5.

Endocrinology
|May 19, 2011
PubMed

Insights

The tumor suppressor p53 inhibits cancer cell migration and invasion by inducing Growth Differentiation Factor-15 (GDF-15) expression. GDF-15 mediates this effect through autocrine/paracrine signaling, reducing cell motility without impacting proliferation.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The p53 tumor suppressor is crucial for cell cycle regulation and apoptosis.
  • p53 also influences cancer cell migration, invasion, and metastasis.
  • Growth Differentiation Factor-15 (GDF-15) is a TGF-β superfamily member, a p53 target, and implicated in cancer progression.

Purpose of the Study:

  • To investigate the role of GDF-15 in p53-mediated cancer cell motility.
  • To elucidate the mechanism by which p53 regulates cancer cell movement.

Main Methods:

  • Overexpression of wild-type p53 in p53-null cancer cell lines (SKOV3, PC3).
  • Assessment of cell migration and Matrigel invasion assays.
  • Utilized wild-type p53 and DNA-binding-deficient mutants to study transcriptional activity.
  • Treatment with recombinant GDF-15 and GDF-15 small interfering RNA (siRNA).

Main Results:

  • Wild-type p53 overexpression attenuated cancer cell migration and Matrigel invasion.
  • p53's transcriptional activity is essential for inducing GDF-15 expression.
  • Recombinant GDF-15 reduced cell movement but did not affect proliferation.
  • GDF-15 siRNA diminished p53-induced GDF-15 expression and reduced cell motility.

Conclusions:

  • p53 attenuates cancer cell motility through the induction of GDF-15 expression.
  • GDF-15 acts via autocrine/paracrine signaling to mediate p53's effects on cell motility.
  • This pathway represents a novel mechanism for p53 in controlling cancer metastasis.

More Related Videos

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

The Soft Agar Colony Formation Assay08:01

The Soft Agar Colony Formation Assay

Published on: October 27, 2014

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.
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...
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...