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Related Concept Videos

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.
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.
Nociception01:44

Nociception

Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain. Thus, pain helps the...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...

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Related Experiment Video

Updated: Jul 7, 2026

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

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NSAIDs and apoptosis.

N R Jana1

  • 1Cellular and Molecular Neuroscience Laboratory, National Brain Research Centre, Manesar, Gurgaon, India. nihar@nbrc.ac.in

Cellular and Molecular Life Sciences : CMLS
|February 23, 2008
PubMed
Summary

Regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin can prevent gastrointestinal cancers by triggering apoptosis. This review explores the COX-2-dependent and independent pathways involved in NSAID-induced cell death.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, are linked to reduced gastrointestinal cancer rates.
  • The chemopreventive effects of NSAIDs are attributed to their capacity to induce apoptosis (programmed cell death).

Purpose of the Study:

  • To review recent literature on the mechanisms of NSAID-induced apoptosis.
  • To elucidate the role of both COX-2-dependent and COX-2-independent pathways in NSAID-mediated cancer prevention.

Main Methods:

  • Literature review of scientific articles.
  • Analysis of studies investigating NSAID mechanisms in cancer chemoprevention.
  • Focus on apoptosis induction pathways.

Main Results:

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

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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
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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

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  • NSAIDs effectively induce apoptosis in neoplastic cells.
  • Both cyclooxygenase-2 (COX-2) dependent and independent pathways contribute to NSAID-induced apoptosis.
  • Understanding these mechanisms is crucial for cancer chemoprevention strategies.

Conclusions:

  • NSAIDs possess significant chemopreventive properties against gastrointestinal cancers.
  • Apoptosis induction is a key mechanism underlying NSAID efficacy.
  • Further research into COX-2-dependent and independent pathways can optimize cancer prevention strategies.