Related Experiment Video

Updated: May 22, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

Proteasomal insensitivity of apoptin in tumor cells

Henriëtte L Lanz1, Johnny Suijker, Mathieu H M Noteborn

  • 1Department of Molecular Genetics, Leiden Institute of Chemistry, Leiden University, Einsteinweg 55, 2333 CC Leiden, The Netherlands. h.lanz@chem.leidenuniv.nl

Biochemical and Biophysical Research Communications
|May 12, 2012
PubMed

Insights

Viral protein apoptin induces apoptosis in tumor cells. Proteasome inhibitors stabilize apoptin in normal cells, but not tumor cells, indicating tumor cells evade apoptin degradation.

Area of Science:

  • Molecular Biology
  • Virology
  • Cancer Research

Background:

  • Apoptin, a viral protein, selectively induces apoptosis in human tumor cells.
  • In normal cells, apoptin is degraded via proteasomal activity after cytoplasmic aggregation.
  • Tumor cells exhibit resistance to apoptin-induced apoptosis.

Purpose of the Study:

  • To investigate the role of proteasomal degradation in apoptin's selective tumor cell activity.
  • To determine if inhibiting proteasome activity affects apoptin stability in normal versus tumor cells.

Main Methods:

  • Utilizing proteasome inhibitors (bortezomib, Ada-Ahx(3)L(3)VS) to block proteasome activity.
  • Comparing apoptin and p53 protein levels in normal and tumor cells under proteasome inhibition.
  • Analyzing the degradation pathway of apoptin in different cell types.

Main Results:

  • Proteasome inhibition stabilized apoptin levels in normal cells, similar to p53.
  • In tumor cells, proteasome inhibition did not affect apoptin stability.
  • p53 levels were stabilized in both normal and tumor cells upon proteasome inhibition.
  • Apoptin degradation by proteasomes occurs in normal cells but is lost in tumor cells.

Conclusions:

  • Apoptin is degraded by the proteasome in normal human cells.
  • Tumor cells have lost susceptibility to apoptin proteasomal degradation.
  • This selective loss of proteasomal degradation contributes to apoptin's tumor-specific activity.

More Related Videos

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

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

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 Proteasome01:13

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important among these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. This involves participation of a series of enzymes including— E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3 (ubiquitin...
The Proteasome02:18

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important amongst these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. A series of enzymes carry out the ubiquitination of the target proteins - E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3...
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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
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...