Related Experiment Video

Updated: Aug 20, 2026

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

PKCdelta requires p53 for suppression of the transformed phenotype in human colon cancer cells

Gianpaolo Perletti1, Emanuela Marras, Daniela Osti

  • 1Department of Structural and Functional Biology, University of Insubria, Via A. Da Giussano, 12, 21052 Varese/Busto Arsizio, Italy. gianpaolo.perletti@uninsubria.it

Journal of Cellular and Molecular Medicine
|December 17, 2004
PubMed

Insights

Protein Kinase C delta (PKCdelta) suppresses colon cancer, but requires wild-type p53. Overexpressing both PKCdelta and p53 halts tumor cell growth, indicating p53 is crucial for PKCdelta

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Protein Kinase C delta (PKCdelta) has shown tumor suppressor activity in HCT116 colon cancer cells.
  • p21(waf1/cip1) was previously identified as a downstream effector of PKCdelta.

Purpose of the Study:

  • To investigate the role of p53 in mediating the tumor-suppressive effects of PKCdelta in human colon cancer cells.
  • To determine if wild-type p53 is necessary for PKCdelta to inhibit the neoplastic phenotype.

Main Methods:

  • Utilized HCT116 human colon cancer cells with homozygous p53 knockout (p53null).
  • Overexpressed PKCdelta and/or p53 in HCT116 p53null cells and HT29 cells (with mutated p53).
  • Assessed changes in cell morphology and growth properties to evaluate the transformed phenotype.

Main Results:

  • PKCdelta overexpression was ineffective in HCT116 cells lacking p53.
  • Reconstitution of p53 alone did not alter cell phenotype.
  • Co-overexpression of p53 and PKCdelta suppressed the transformed phenotype in HCT116 cells.
  • PKCdelta was also ineffective in HT29 cells harboring a dominant-negative p53 mutation.

Conclusions:

  • Wild-type p53 is an essential mediator of PKCdelta's tumor-suppressive function in human colon cancer.
  • The presence of functional p53 is required for PKCdelta to inhibit neoplastic growth.
  • These findings highlight a critical interplay between p53 and PKCdelta in colon cancer suppression.

More Related Videos

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer08:34

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

Published on: April 13, 2015

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

Related Concept Videos

Abnormal Proliferation02:23

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...
DNA Damage can Stall the Cell Cycle02:36

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 Cycle02:36

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...
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...
Negative Regulator Molecules01:23

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.
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...