Related Experiment Video

Updated: May 11, 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

β-ionone induces cell cycle arrest and apoptosis in human prostate tumor cells

Sheila Jones1, Nicolle V Fernandes, Hoda Yeganehjoo

  • 1Department of Nutrition and Food Sciences, Texas Woman's University, Denton, Texas 76204, USA.

Nutrition and Cancer
|May 11, 2013
PubMed

Insights

Beta-ionone, a dietary isoprenoid, inhibits prostate cancer cell growth by suppressing HMG CoA reductase. This compound, alone or with farnesol, shows promise for prostate cancer chemoprevention and therapy.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • 3-Hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase is crucial for the mevalonate pathway, supplying intermediates for protein modification.
  • Dietary isoprenoids can suppress HMG CoA reductase and exhibit cancer chemopreventive properties.

Purpose of the Study:

  • To investigate the effects of beta-ionone, a cyclic sesquiterpene, on prostate carcinoma and adenocarcinoma cell proliferation.
  • To explore the potential of beta-ionone, individually and in combination with farnesol, for prostate cancer chemoprevention and therapy.

Main Methods:

  • Cell proliferation assays were performed on human prostate cancer cell lines (DU145, LNCaP, PC-3).
  • Apoptosis and cell cycle arrest were analyzed using fluorescence microscopy, flow cytometry, and TUNEL assay.
  • Protein levels of key cell cycle regulators (Cdk4, cyclin D1) and HMG CoA reductase were assessed.

Main Results:

  • Beta-ionone demonstrated concentration-dependent inhibition of proliferation in DU145, LNCaP, and PC-3 cells.
  • Beta-ionone induced apoptosis and G1 phase cell cycle arrest in DU145 and PC-3 cells, accompanied by downregulation of Cdk4 and cyclin D1.
  • A combination of beta-ionone and trans, trans-farnesol exhibited synergistic growth suppression in DU145 cells.

Conclusions:

  • Beta-ionone effectively suppresses prostate cancer cell growth and induces apoptosis and cell cycle arrest.
  • The combination of beta-ionone and farnesol shows enhanced efficacy, suggesting synergistic effects.
  • Beta-ionone holds potential for prostate cancer chemoprevention and therapy, particularly when used with other HMG CoA reductase inhibitors.

Related Concept Videos

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.
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...