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Abnormal Proliferation

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...

Inhibition of Cdk Activity

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...

Inhibition of CDK Activity

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...

Negative Regulator Molecules

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.

DNA Damage can Stall the Cell Cycle

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

DNA Damage Can Stall the Cell Cycle

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

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Related Experiment Video

Updated: Jun 22, 2026

Functionalized Spirocyclic Heterocycle Synthesis and Cytotoxicity Assay

Functionalized Spirocyclic Heterocycle Synthesis and Cytotoxicity Assay

Published on: February 9, 2021

Cyclooxygenase-2 functionally inactivates p53 through a physical interaction with p53.

Eun Mi Choi¹, So Ra Kim, Eun Jeong Lee

¹Department of Biochemistry and Molecular Biology, Kangwon National University College of Medicine, Chuncheon 200-701, South Korea.

Biochimica Et Biophysica Acta

|May 26, 2009

Summary

Cyclooxygenase-2 (COX-2) physically interacts with the tumor suppressor p53 in the nucleus upon genotoxic stress. This interaction inhibits p53

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Functionalized Spirocyclic Heterocycle Synthesis and Cytotoxicity Assay

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Published on: August 4, 2019

Area of Science:

Molecular Biology
Cancer Research
Cell Biology

Background:

Cyclooxygenase-2 (COX-2) is implicated in tumorigenesis.
The precise mechanisms of COX-2 in promoting cancer are not fully understood.
Previous studies indicated a physical interaction between COX-2 and p53.

Purpose of the Study:

To elucidate the mechanism by which COX-2 interacts with p53.
To determine if this interaction regulates p53 function.
To investigate the role of COX-2-p53 interaction in tumorigenesis.

Main Methods:

Investigated COX-2 and p53 localization and interaction under genotoxic stress.
Utilized co-immunoprecipitation and functional assays to study protein interactions.
Employed site-directed mutagenesis to identify critical interaction domains.

Main Results:

COX-2 and p53 co-localize and interact in the nucleus following genotoxic stress.
An N-terminal region of COX-2 (amino acids 1-126) binds to the p53 DNA-binding domain.
This interaction inhibits p53 DNA-binding, transcriptional activity, and apoptosis in a catalytic-independent manner.

Conclusions:

COX-2 inhibits p53 function through nuclear physical interaction, independent of its catalytic activity.
This inhibition of p53 by COX-2 is a key mechanism promoting tumorigenesis.
Findings offer new insights into COX-2's role in cancer development.