Related Experiment Video
Updated: Jun 28, 2026

Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation
Published on: December 26, 2017
Anti-metastatic action of non-steroidal anti-inflammatory drugs
1Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan. hung1228@ms10.hinet.net
Abstract:
Epidemiological studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the incidence and mortality of several types of human cancer. However, the molecular mechanisms by which NSAIDs exert their chemopreventive and anticancer effects are not fully understood. Cyclooxygenase 1 (COX-1) and COX-2 are the main targets for NSAIDs. Recent studies demonstrate that COX-2 is overexpressed in many human cancers and may promote tumorigenesis via: (1) stimulation of cancer cell proliferation; (2) increase of tumor angiogenesis; (3) prevention of cancer cell apoptosis; (4) modulation of immunoregulatory reactions; and (5) enhancement of tumor metastasis. NSAIDs may target the signaling molecules (from upstream activators to downstream effectors) involved in these mechanisms to attenuate the development and progression of cancer. In this review, we discuss the recent findings with regard to the mechanisms by which NSAIDs inhibit tumorigenesis and will specifically focus on the elucidation of NSAID-induced inhibition of tumor metastasis.
Insights
Nonsteroidal anti-inflammatory drugs (NSAIDs) may prevent cancer by targeting mechanisms like cell proliferation and metastasis. Further research clarifies how NSAIDs inhibit tumor development and progression, particularly metastasis.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Epidemiological studies indicate nonsteroidal anti-inflammatory drugs (NSAIDs) reduce cancer incidence and mortality.
- The precise molecular mechanisms underlying NSAID chemoprevention and anticancer effects remain incompletely understood.
- Cyclooxygenase-2 (COX-2) is frequently overexpressed in cancers and implicated in tumorigenesis.
Purpose of the Study:
- To review recent findings on the mechanisms of NSAID-mediated cancer inhibition.
- To elucidate how NSAIDs attenuate cancer development and progression.
- To specifically focus on NSAID-induced inhibition of tumor metastasis.
Main Methods:
- Review of current scientific literature and studies.
- Analysis of molecular pathways targeted by NSAIDs.
- Focus on COX-1 and COX-2 as primary NSAID targets.
Main Results:
- COX-2 overexpression promotes tumorigenesis through proliferation, angiogenesis, apoptosis evasion, immune modulation, and metastasis.
- NSAIDs may counteract these pro-tumorigenic effects by targeting relevant signaling molecules.
- Evidence suggests NSAIDs can inhibit key steps in tumor metastasis.
Conclusions:
- NSAIDs possess significant potential for cancer chemoprevention and treatment.
- Targeting COX pathways offers a promising strategy for cancer therapy.
- Understanding NSAID mechanisms, especially regarding metastasis, is crucial for developing effective anticancer drugs.
More Related Videos
Related Concept Videos
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents
Antibody Actions
Neutralization
Antibodies can bind to pathogens, preventing them from infecting host cells. This process...
Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

