Related Experiment Video

Updated: Jun 3, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

The hallmarks of CDKN1C (p57, KIP2) in cancer

Edel Kavanagh1, Bertrand Joseph

  • 1Department of Oncology-Pathology, Cancer Centrum Karolinska, Stockholm, Sweden. Edel.Kavanagh@ki.se

Biochimica Et Biophysica Acta
|March 31, 2011
PubMed

Insights

Cyclin-dependent kinase inhibitor 1C (p57KIP2) is a tumor suppressor often epigenetically silenced in cancer. Reactivating p57KIP2 offers therapeutic potential and prognostic value across various cancer types.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Cyclin-dependent kinase inhibitor 1C (p57KIP2) is a key regulator of cancer hallmarks.
  • p57KIP2 functions as a tumor suppressor by influencing apoptosis, cell invasion, metastasis, differentiation, and angiogenesis.
  • Unlike many cancer genes, p57KIP2 is typically not mutated but epigenetically silenced.

Purpose of the Study:

  • To review the multifaceted tumor suppressor functions of p57KIP2.
  • To elucidate the mechanisms of p57KIP2 transcriptional repression in cancer.
  • To explore the therapeutic potential of reactivating p57KIP2 gene expression.

Main Methods:

  • This review synthesizes existing literature on p57KIP2.
  • Mechanisms of epigenetic regulation (DNA methylation, histone modification) are discussed.
  • The role of p57KIP2 as a prognostic biomarker is examined.

Main Results:

  • p57KIP2 expression is frequently downregulated in cancer via epigenetic silencing.
  • Epigenetic repression mechanisms include promoter DNA methylation and repressive histone marks.
  • p57KIP2 demonstrates prognostic value in various cancers, distinguishing early from late stages.

Conclusions:

  • Reactivation of p57KIP2 gene expression presents a promising therapeutic strategy.
  • Understanding p57KIP2 repression mechanisms is crucial for developing targeted therapies.
  • p57KIP2 serves as a valuable prognostic factor in cancer management.

More Related Videos

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

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...
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...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
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...