Related Experiment Video

Updated: Apr 26, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

6.8K

Selective repression of the oncogene cyclin D1 by the tumor suppressor miR-206 in cancers

S J Elliman1, B V Howley2, D S Mehta3

  • 1Orbsen Therapeutics Ltd, Galway, Ireland.

Oncogenesis
|August 12, 2014
PubMed

Insights

MicroRNA-206 (miR-206) inhibits cyclin D1, a cancer-promoting gene, leading to cell cycle arrest and reduced proliferation in breast cancer cells. This suggests miR-206 as a potential therapeutic target for cancers with high cyclin D1 expression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • MicroRNAs (miRNAs) play crucial roles in cancer, acting as either oncogenes or tumor suppressors.
  • The specific functions of many miRNAs, including their roles in cell cycle regulation, remain largely uncharacterized.

Purpose of the Study:

  • To investigate the role of microRNA-206 (miR-206) in regulating cyclin D1 expression and its impact on cell proliferation.
  • To explore the potential of miR-206 as a therapeutic agent in cancers characterized by cyclin D1 overexpression.

Main Methods:

  • In silico analysis to identify miR-206 binding sites in the CCND1 gene's 3'-untranslated region (3'-UTR).
  • Experimental validation of miR-206 binding and its effect on cyclin D1 protein and mRNA levels in breast cancer cells.
  • Assessment of cell cycle progression and proliferation following miR-206 expression and manipulation of cyclin D1.

Main Results:

  • miR-206 directly binds to the CCND1 3'-UTR, reducing both cyclin D1 mRNA and protein levels.
  • Overexpression of miR-206 induces G1 cell cycle arrest and decreases proliferation in breast cancer cells.
  • Prostatic cancer cells exhibit low miR-206 levels and lack the CCND1 3'-UTR, rendering them resistant to miR-206-mediated cyclin D1 regulation.

Conclusions:

  • miR-206 acts as a tumor suppressor by inhibiting cyclin D1, thereby inducing cell cycle arrest and reducing proliferation.
  • The absence of the CCND1 3'-UTR in prostatic cancer cells explains their resistance to miR-206 regulation.
  • Targeted miR-206 therapy holds promise for cancers with overexpressed cyclin D1 and an intact 3'-UTR.

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

7.1K
Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis07:26

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis

Published on: January 31, 2025

1.1K

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...
4.8K
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

4.3K
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.
5.3K
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
100.8K
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...
5.3K
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.
32.1K