Related Experiment Video

Updated: Jun 20, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

Quercetin-induced apoptosis acts through mitochondrial- and caspase-3-dependent pathways in human breast cancer

Su-Yu Chien1, Yao-Chung Wu, Jing-Gung Chung

  • 1Department of Pharmacology, Changhua Christian Hospital, 135 Nanhsiao St., Changhua, Taiwan.

Human & Experimental Toxicology
|September 17, 2009
PubMed

Insights

Quercetin, a natural flavonol, effectively reduces human breast cancer cell viability by triggering apoptosis. This occurs via mitochondrial pathways and caspase activation, offering a potential therapeutic strategy.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Flavonols, including quercetin, exhibit anti-tumour properties.
  • Quercetin inhibits cancer cell proliferation and induces apoptosis.
  • The exact mechanism of quercetin-induced apoptosis in breast cancer is not fully understood.

Purpose of the Study:

  • Investigate quercetin's effects on human breast cancer MDA-MB-231 cell viability.
  • Elucidate the molecular mechanisms underlying quercetin-induced apoptosis.

Main Methods:

  • Cell viability assays (dose- and time-dependent).
  • Cell cycle analysis.
  • Measurement of reactive oxygen species (ROS) and cytosolic Ca(2+) levels.
  • Mitochondrial membrane potential (ΔΨm) assessment.
  • Caspase activation assays (caspase-3, -8, -9).
  • Western blot analysis for Bax and Bcl-2 protein levels.
  • Confocal microscopy for apoptosis-inducing factor (AIF) translocation.

Main Results:

  • Quercetin significantly decreased MDA-MB-231 cell viability.
  • Apoptosis was induced, evidenced by cell cycle arrest and altered Bax/Bcl-2 ratios.
  • Quercetin increased cytosolic Ca(2+) and reduced ΔΨm, without increasing ROS.
  • Activation of caspase-3, -8, and -9 was observed.
  • Caspase inhibitors partially blocked quercetin's cytotoxic effect.
  • AIF was released from mitochondria and translocated to the nucleus.

Conclusions:

  • Quercetin induces apoptosis in human breast cancer MDA-MB-231 cells.
  • The mechanism involves mitochondrial dysfunction and caspase-3 activation.
  • Quercetin's effects are mediated by AIF release and nuclear translocation.

More Related Videos

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling08:51

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling

Published on: June 25, 2015

Related Concept Videos

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...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
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...