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Related Concept Videos

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.
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...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
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...
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...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

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Related Experiment Video

Updated: May 16, 2026

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death
13:54

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death

Published on: October 21, 2012

E2F1 apoptosis counterattacked: evil strikes back.

Brigitte M Pützer1, David Engelmann

  • 1Department of Vectorology and Experimental Gene Therapy, Biomedical Research Center, Rostock University Medical Center Schillingallee 69, 18057 Rostock, Germany. brigitte.puetzer@med.uni-rostock.de

Trends in Molecular Medicine
|December 11, 2012
PubMed
Summary
This summary is machine-generated.

High E2F1 levels in late-stage cancers promote tumor invasion and metastasis, not apoptosis. Understanding how cancer cells evade E2F1-induced apoptosis reveals new therapeutic strategies for drug resistance.

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Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death
13:54

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Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
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Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis

Published on: June 27, 2020

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Cancer therapy failure is often due to drug resistance.
  • E2F1 (E2F transcription factor 1) was previously known as a key regulator of apoptosis (programmed cell death).
  • Recent evidence shows E2F1 is aberrantly high in late-stage cancers, promoting invasion and metastasis instead of apoptosis.

Purpose of the Study:

  • To elucidate the molecular mechanisms counteracting E2F1-induced apoptosis in cancer cells.
  • To explain the paradox of high E2F1 expression in advanced tumors.
  • To identify novel therapeutic strategies for overcoming cancer drug resistance.

Main Methods:

  • Review of recent advances in molecular mechanisms.
  • Focus on E2F1 signaling pathways in damaged cells.
  • Analysis of cell context-dependent functions of E2F1.

Main Results:

  • Deregulated E2F1 exhibits context-dependent loss of its death-inducing function.
  • Specific molecular mechanisms enable cancer cells to evade E2F1-mediated apoptosis.
  • High E2F1 expression in advanced cancers facilitates tumor invasion and metastasis.

Conclusions:

  • The dual role of E2F1 in cancer, promoting survival and metastasis under specific conditions, explains treatment failure.
  • Understanding these evasion mechanisms offers potential therapeutic targets.
  • Novel strategies can be developed to re-sensitize resistant cancers to genotoxic drugs.