Related Experiment Video

Updated: Jun 12, 2026

Proximity Ligand Assay to Localize Proteins in DNA Damage Sites
09:39

Proximity Ligand Assay to Localize Proteins in DNA Damage Sites

Published on: August 2, 2024

p73 participates in male germ cells apoptosis induced by etoposide

Verónica A Codelia1, Matías Cisterna, Alejandra R Alvarez

  • 1Departamento de Ciencias Fisiológicas, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.

Molecular Human Reproduction
|June 4, 2010
PubMed

Insights

The c-Abl/p73 pathway activates germ cell apoptosis following etoposide treatment in testicular cancer. Inhibiting this pathway reduces cell death, suggesting a new therapeutic target.

Area of Science:

  • Molecular Biology
  • Cell Death Research
  • Cancer Therapeutics

Background:

  • Etoposide is a key chemotherapy for testicular cancer, but its mechanism of germ cell apoptosis induction is unclear.
  • Understanding these pathways is crucial for improving treatment efficacy and minimizing side effects.

Purpose of the Study:

  • To investigate the role of p73, a p53 family member, in etoposide-induced apoptosis in male germ cells.
  • To elucidate the involvement of the c-Abl kinase in this process.

Main Methods:

  • Utilized GC2-spc cells (male germ cell model) and in vivo rat testes models.
  • Assessed protein levels (p73, c-Abl, phospho-p73), cell viability, and caspase activation.
  • Employed etoposide treatment, Pifithrin (PFT), STI571 (c-Abl inhibitor), and shRNA knockdown (p73/p53).

Main Results:

  • Etoposide increased p73 and c-Abl levels, decreased cell viability, and activated caspase-3 in GC2-spc cells.
  • PFT and p73/p53 knockdown inhibited etoposide-induced apoptosis.
  • In vivo, etoposide upregulated p73 and phospho-p73; co-administration of STI571 or PFT reduced apoptosis and caspase activation.

Conclusions:

  • The c-Abl/p73 pathway is activated by etoposide in male germ cells, leading to apoptosis.
  • This pathway may act in concert with p53, offering potential therapeutic targets for testicular cancer treatment.

More Related Videos

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method09:32

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

Published on: September 10, 2017

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

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...
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...
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...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...