Related Experiment Video

Updated: Jun 9, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Overexpression of ornithine decarboxylase suppresses thapsigargin-induced apoptosis

Wei-Chung Hsieh1, Pei-Chen Hsu, Ya-Fan Liao

  • 1Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan, ROC.

Molecules and Cells
|September 4, 2010
PubMed

Insights

Overexpression of ornithine decarboxylase (ODC) inhibits endoplasmic reticulum (ER) stress-induced apoptosis. ODC overexpression blocks key apoptotic pathways, protecting cells from thapsigargin-induced cell death.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Ornithine decarboxylase (ODC) is crucial for polyamine biosynthesis and has complex roles in apoptosis.
  • Overexpression of ODC has been shown to prevent apoptosis induced by various cytotoxic drugs.
  • Thapsigargin (TG) induces apoptosis via endoplasmic reticulum (ER) stress by inhibiting SERCA pumps.

Purpose of the Study:

  • To investigate the effect of ODC overexpression on thapsigargin (TG)-induced apoptosis.
  • To elucidate the molecular mechanisms by which ODC influences ER stress-induced apoptosis.

Main Methods:

  • Utilized ODC overexpressing cell lines.
  • Analyzed procaspase-4 cleavage, PERK phosphorylation, and CHOP expression.
  • Assessed Bcl-2 and Bak expression, mitochondrial membrane potential, and cytochrome c release.
  • Examined SERCA protein and mRNA expression.

Main Results:

  • ODC overexpression attenuated TG-induced apoptosis.
  • Blocked procaspase-4 cleavage and PERK phosphorylation, and attenuated CHOP increase.
  • Preserved Bcl-2 expression, inhibited Bak increase, and stabilized mitochondrial membrane potential.
  • Inhibited cytochrome c release and downstream caspase activation, thus blocking the mitochondria-mediated apoptotic pathway.
  • Maintained SERCA protein and mRNA expression.

Conclusions:

  • Overexpression of ODC suppresses TG-induced apoptosis.
  • This suppression occurs by inhibiting caspase-4 activation and PERK phosphorylation.
  • ODC overexpression attenuates CHOP expression and the mitochondria-mediated apoptotic pathway.

More Related Videos

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries08:49

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Related Concept Videos

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...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
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...
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...