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Related Concept Videos

Molecular Factors Affecting Cell Division01:27

Molecular Factors Affecting Cell Division

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Several external and internal factors influence the initiation and inhibition of cell division. For instance, the death of nearby cells or the release of human growth hormone (hGH) promotes cell division. In contrast, lack of hGH or crowding of cells can inhibit cell division.
Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...
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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...
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The Cell Cycle Control System01:28

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The cell cycle regulation directs how a cell proceeds from one phase to the next and begins mitosis. The cell cycle control system includes intracellular regulatory molecules and external triggers. They provide "stop" or "advance" signals and operate at specific cell cycle stages termed checkpoints to ensure that a particular process is completed before the cell advances to the next phase.
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The cell cycle is an organized set of events that leads the cell to divide into two daughter cells, each containing chromosomes identical to the parent cell. It is the cell cycle that leads to the formation of an entire organism from a single-cell zygote. Besides, cell division also functions in the renewal or repair of tissues in adult multicellular eukaryotes. For example, in the bone marrow, the stem cells divide to form new blood cells. Although essential for several functions, cell...
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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.
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To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
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Related Experiment Video

Updated: Mar 6, 2026

Isolation and Staining of Mouse Skin Keratinocytes for Cell Cycle Specific Analysis of Cellular Protein Expression by Mass Cytometry
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Isolation and Staining of Mouse Skin Keratinocytes for Cell Cycle Specific Analysis of Cellular Protein Expression by Mass Cytometry

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Cell-Cycle Regulation Accounts for Variability in Ki-67 Expression Levels.

Michal Sobecki1, Karim Mrouj1, Jacques Colinge2

  • 1IGMM, CNRS Univ. Montpellier, Montpellier, France.

Cancer Research
|March 12, 2017
PubMed
Summary
This summary is machine-generated.

Cell-cycle regulation explains variable Ki-67 expression in cancer and normal cells. Ki-67 reliably indicates CDK4/CDK6 inhibitor effects on cell proliferation.

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Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • The cell proliferation marker Ki-67 is crucial in cancer histopathology.
  • Inconsistent Ki-67 expression estimations and limited understanding of its regulation pose challenges.

Purpose of the Study:

  • To investigate the role of cell-cycle regulation in Ki-67 expression variability.
  • To determine if Ki-67 remains a reliable proliferation marker under CDK4/CDK6 inhibition.

Main Methods:

  • Analysis of Ki-67 expression in various cell types and tissues (human and mouse).
  • Investigated Ki-67 mRNA and protein dynamics throughout the cell cycle.
  • Utilized CDK4/CDK6 inhibition (in vitro and in vivo) to assess Ki-67 regulation and response.

Main Results:

  • Cell-cycle regulation was identified as the primary driver of Ki-67 expression variability across all analyzed conditions.
  • Ki-67 mRNA levels peaked in G2, while protein levels increased through the cell cycle, peaking in mitosis.
  • CDK4/CDK6 inhibition induced G1 arrest and eliminated Ki-67 mRNA in RB1-positive cells, but not in RB1-negative cells.

Conclusions:

  • Ki-67 expression is intrinsically linked to cell-cycle progression and regulation.
  • Despite variability, Ki-67 remains a dependable indicator for evaluating the efficacy of CDK4/CDK6 inhibitors in targeting cell proliferation.