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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...

Positive Regulator Molecules

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.

Positive Regulator Molecules

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.

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.

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...

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Related Experiment Video

Updated: May 19, 2026

The Soft Agar Colony Formation Assay

The Soft Agar Colony Formation Assay

Published on: October 27, 2014

CDCA7 Promotes Neuroblastoma Proliferation via Regulating the Cell Cycle.

Wen Yuan¹, Xiaoxing Huang², Renwei Luo³

¹Department of Laboratory Medicine, Wuhan Children's Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430016, China.

Iranian Journal of Biotechnology

|May 18, 2026

Summary

This summary is machine-generated.

Cell division cycle-associated 7 (CDCA7) is overexpressed in neuroblastoma (NB) and linked to poor survival. Silencing CDCA7 inhibits NB cell proliferation by causing G1 cell cycle arrest and reducing CDK6 expression.

Keywords:

CDCA7 CDK6 Cell cycle Neuroblastoma Proliferation

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Last Updated: May 19, 2026

The Soft Agar Colony Formation Assay

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Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells (NPCs)

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Published on: March 2, 2018

Area of Science:

Oncology
Molecular Biology
Cancer Research

Background:

Cell division cycle-associated 7 (CDCA7) is implicated in various cancers, but its role in neuroblastoma (NB) remains undefined.
Understanding CDCA7's function in NB is crucial for developing targeted therapies.

Purpose of the Study:

To investigate the expression, clinical significance, and biological functions of CDCA7 in neuroblastoma.
To elucidate the molecular mechanisms by which CDCA7 regulates NB cell proliferation and cell cycle progression.

Main Methods:

Analysis of NB datasets to assess CDCA7 expression and correlation with clinical features.
In vitro studies involving CDCA7 knockdown using shRNA, cell proliferation assays (CCK8), cell cycle analysis (flow cytometry), and molecular analysis (qPCR, Western blotting).
Evaluation of CDCA7's association with immune cell infiltration.

Main Results:

CDCA7 is highly expressed in NB tissues and cell lines, with elevated levels in MYCN-amplified NB and advanced stages.
High CDCA7 expression correlates with poor overall survival (OS) and event-free survival (EFS) in NB patients.
CDCA7 knockdown suppressed proliferation, induced G1 cell cycle arrest, and decreased CDK6 expression, while also showing associations with immune cell infiltration (B cells, CD4+ T cells, macrophages).

Conclusions:

CDCA7 serves as a potential prognostic biomarker for neuroblastoma.
CDCA7 inhibition results in G1 cell cycle arrest and reduced CDK6 expression, thereby inhibiting NB cell proliferation.
CDCA7 influences the tumor microenvironment through its association with immune cell infiltration.