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Inhibition of Cdk Activity

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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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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.
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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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The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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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...
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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
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MYC Modulation around the CDK2/p27/SKP2 Axis.

Per Hydbring1, Alina Castell2, Lars-Gunnar Larsson3

  • 1Department of Oncology-Pathology, Karolinska Institutet, SE-171 76 Stockholm, Sweden. per.hydbring@ki.se.

Genes
|July 1, 2017
PubMed
Summary
This summary is machine-generated.

The MYC transcription factor forms a critical network with cell cycle regulators, including cyclin-dependent kinase 2 (CDK2), p27, and SKP2. This intricate interplay influences cell proliferation, survival, and cancer development.

Keywords:
cancercell cyclecellular senescenceoncogenesphosphorylationpost-translational modificationsprotein–protein interactionsthe ubiquitin/proteasome systemtranscriptiontumor suppressor genes

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • The MYC transcription factor is crucial for cell proliferation and survival in both normal and malignant cells.
  • MYC regulates fundamental cellular processes, including the cell cycle, by interacting with key regulators.

Purpose of the Study:

  • To elaborate on the network interactions between MYC and cell cycle regulators.
  • To investigate the impact of these interactions on transcription, cell cycle progression, replication, and stress signaling.
  • To discuss the therapeutic potential of targeting the MYC/CDK2/p27/SKP2 axis in cancer treatment.

Main Methods:

  • Review and elaboration of existing literature on MYC network interactions.
  • Analysis of the bidirectional crosstalk between MYC and cell cycle regulators (CDK2, p27, SKP2).
  • Discussion of interconnected players like CDK1, pRB, PP2A, FBXW7, FBXO28, RAS, and the ubiquitin/proteasome system.

Main Results:

  • MYC engages in bidirectional crosstalk with CDK2, p27, and SKP2, forming a regulatory network.
  • These interactions modulate MYC's transcriptional output and impact cell cycle control and senescence.
  • The MYC/CDK2/p27/SKP2 axis plays a significant role in tumor development.

Conclusions:

  • The MYC-centric network involving CDK2, p27, and SKP2 is vital for cell cycle regulation and cancer progression.
  • Understanding these interactions offers potential therapeutic strategies for cancer treatment.
  • Targeting this axis could provide novel avenues for improving cancer therapy.