Related Experiment Video

Updated: Sep 20, 2026

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
00:06

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

Published on: September 12, 2019

Hepatocellular carcinoma: is there a potential for chemoprevention using cyclooxygenase-2 inhibitors?

Hironori Koga1

  • 1Second Department of Medicine, and Kurume University Research Center for Innovative Cancer Therapy, Kurume University, Kurume, Japan. hirokoga@med.kurume-u.ac.jp

Cancer
|August 12, 2003
PubMed

Insights

Selective cyclooxygenase-2 (COX-2) inhibitors may prevent liver cancer by reducing tumor growth and spread. Further animal studies are needed to confirm their potential for cancer prevention.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Cyclooxygenase-2 (COX-2) inhibitors exhibit anti-tumor effects, including apoptosis induction and anti-angiogenesis.
  • These effects are mediated through both COX-dependent and COX-independent pathways, involving peroxisome proliferator-activated receptor gamma.
  • The specific role of COX-2 in human liver cancer (hepatocarcinogenesis) remains unclear.

Purpose of the Study:

  • To explore the potential of selective COX-2 inhibitors, particularly those with COX-independent activity, in suppressing hepatocarcinogenesis.
  • To propose the need for in vivo validation of this hypothesis using animal models.

Main Methods:

  • This study is a hypothesis-driven review and proposal for future research.
  • It discusses the known mechanisms of COX-2 inhibitors and their relevance to liver cancer.

Main Results:

  • Selective COX-2 inhibitors possess properties that could inhibit malignant tumor growth and invasion.
  • COX-independent signaling pathways offer a potential mechanism for anti-cancer effects.

Conclusions:

  • Selective COX-2 inhibitors with COX-independent properties may hold promise for preventing liver cancer.
  • In vivo studies are crucial to confirm the efficacy of COX-2 inhibitors in hepatocarcinogenesis and explore their chemopreventive applications.

More Related Videos

A Three-Dimensional Spheroid Model to Investigate the Tumor-Stromal Interaction in Hepatocellular Carcinoma12:24

A Three-Dimensional Spheroid Model to Investigate the Tumor-Stromal Interaction in Hepatocellular Carcinoma

Published on: September 30, 2021

Structure-Guided Design and Development of Novel Cyclophilin A Inhibitors and Ganoderiol-F Derivatives: An In-Silico Approach10:01

Structure-Guided Design and Development of Novel Cyclophilin A Inhibitors and Ganoderiol-F Derivatives: An In-Silico Approach

Published on: June 23, 2026

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Cancer Prevention02:59

Cancer Prevention

Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
Some...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...