Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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.
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.
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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Bcl-2 modifying factor (Bmf): "a mysterious stranger" in the Bcl-2 family proteins.

Cell death and differentiation·2025
Same author

Prognostic model integrating histology, systemic inflammation, and recurrence status predicts immunotherapy response in advanced non-small-cell lung cancer patients.

Biology direct·2025
Same author

Correction: p73 and caspase-cleaved p73 fragments localize to mitochondria and augment TRAIL-induced apoptosis.

Oncogene·2025
Same author

BH3-mimetics or DNA-damaging agents in combination with RG7388 overcome p53 mutation-induced resistance to MDM2 inhibition.

Apoptosis : an international journal on programmed cell death·2024
Same author

Bcl-B: an "unknown" protein of the Bcl-2 family.

Biology direct·2023
Same author

Rapid, sensitive, and specific, low-resource molecular detection of Hendra virus.

One health (Amsterdam, Netherlands)·2023
Same journal

A planar dimer of bovine ATP synthase.

Cell death and differentiation·2026
Same journal

GCN5 and TADA2B constitutively regulate XRCC1 function during DNA repair to maintain cell survival.

Cell death and differentiation·2026
Same journal

MEGF8 controls osteogenic differentiation through post-transcriptional regulation of BMP-SMAD signaling in craniosynostosis.

Cell death and differentiation·2026
Same journal

Macrophage-secreted brain-derived neurotrophic factor promotes tumor growth in triple-negative breast cancer by inducing axonogenesis.

Cell death and differentiation·2026
Same journal

Species-specific regulation of necroptosis by STK38-dependent RIPK1 phosphorylation.

Cell death and differentiation·2026
Same journal

Ssu72 phosphatase orchestrates obesogenic adipogenesis and metabolic homeostasis during nutrient excess.

Cell death and differentiation·2026
See all related articles

Related Experiment Video

Updated: Jun 3, 2026

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation
08:47

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Published on: March 5, 2018

Caspases and cancer.

M Olsson1, B Zhivotovsky

  • 1Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Cell Death and Differentiation
|April 2, 2011
PubMed
Summary
This summary is machine-generated.

Cancer cells evade apoptosis, a key cell death process regulated by caspases. This review explores if caspase deregulation, not just insufficient activation, drives tumor growth by promoting cell survival.

More Related Videos

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila
13:21

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila

Published on: November 27, 2016

Measuring Caspase Activity Using a Fluorometric Assay or Flow Cytometry
05:29

Measuring Caspase Activity Using a Fluorometric Assay or Flow Cytometry

Published on: March 24, 2023

Related Experiment Videos

Last Updated: Jun 3, 2026

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation
08:47

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Published on: March 5, 2018

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila
13:21

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila

Published on: November 27, 2016

Measuring Caspase Activity Using a Fluorometric Assay or Flow Cytometry
05:29

Measuring Caspase Activity Using a Fluorometric Assay or Flow Cytometry

Published on: March 24, 2023

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cell Death Pathways

Background:

  • Evasion of apoptosis is a hallmark of human cancers.
  • Apoptosis is executed by caspases, with upstream regulators acting as tumor suppressors or oncogenes.
  • Regulatory factors involved in apoptosis also play roles in cell survival and repair pathways.

Purpose of the Study:

  • To investigate if deregulation of specific caspases, rather than insufficient caspase activation, contributes to tumor formation.
  • To examine the evidence linking caspase malfunction to enhanced tumorigenic potential through inappropriate cell survival.

Main Methods:

  • Review of basic molecular mechanisms from in vitro analyses.
  • Emphasis on new insights from in vivo and clinical studies.

Main Results:

  • Caspases possess tumor suppressor functions.
  • Redundancy in caspase regulatory functions and substrate recognition exists.
  • Deregulation of specific caspases may lead to enhanced tumorigenic potential.

Conclusions:

  • While caspases are crucial for apoptosis, their specific deregulation, not solely insufficient activation, is implicated in cancer progression.
  • Further research integrating in vitro, in vivo, and clinical data is needed to fully understand the role of caspase deregulation in tumorigenesis.