Related Experiment Video

Updated: Jun 16, 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

Restoration of p53 functions protects cells from concanavalin A-induced apoptosis

A R M Ruhul Amin1, Vijay S Thakur, Kalpana Gupta

  • 1Department of Genetics, Case Western Reserve University, Cleveland, Ohio 44106, USA.

Molecular Cancer Therapeutics
|February 4, 2010
PubMed

Insights

Concanavalin A (Con A) induces cancer cell death by activating FOXO1a-Bim signaling in cells lacking p53. Wild-type p53 protein protects cells by halting cell cycle and downregulating FOXO1a and Bim, revealing a new p53-FOXO1a interaction.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Biology

Background:

  • The p53 network is frequently disrupted in human cancers, making its components key targets for novel cancer therapies.
  • Understanding p53-dependent and independent apoptosis pathways is crucial for developing effective treatments.
  • Concanavalin A (Con A) was previously shown to induce p73-dependent apoptosis in p53-deficient cells.

Purpose of the Study:

  • To investigate the protective role of p53 against Con A-induced apoptosis.
  • To elucidate the molecular mechanisms underlying p53-mediated protection from Con A.
  • To identify novel cross-talk between p53 and other key signaling pathways.

Main Methods:

  • Utilized p53-null and wild-type p53 isogenic cancer cell lines (SKOV3, MDAH041, SKP53, TR9-7).
  • Treated cells with Concanavalin A (Con A) and assessed apoptosis.
  • Inhibited p53 function and ablated Bim expression using short hairpin RNA (shRNA).
  • Analyzed the expression of FOXO1a and Bim proteins via Western blotting.

Main Results:

  • Con A induced apoptosis in p53-null cells, while wild-type p53-expressing cells were protected by G(1) arrest.
  • Inhibition of p53 function sensitized cells to Con A-induced apoptosis.
  • Con A upregulated FOXO1a and Bim, which were downregulated by p53 expression and upregulated upon p53 ablation.
  • Ablation of Bim significantly protected cells from Con A-induced apoptosis.

Conclusions:

  • Con A triggers apoptosis in p53-deficient cells via the FOXO1a-Bim signaling pathway.
  • Wild-type p53 confers resistance to Con A by inducing G(1) arrest and suppressing FOXO1a and Bim expression.
  • A novel cross-talk between FOXO1a and p53 transcription factors in regulating apoptosis has been identified.

More Related Videos

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

Purification of Ubiquitinated p53 Proteins from Mammalian Cells10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Related Concept Videos

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...
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.
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...