Related Experiment Video

Updated: Nov 24, 2025

Author Spotlight: Investigating the Potential of Chinese Herbal Medicinal Active Dioscin in Treating IgA Nephropathy
14:18

Author Spotlight: Investigating the Potential of Chinese Herbal Medicinal Active Dioscin in Treating IgA Nephropathy

Published on: October 13, 2023

2.1K

Dioscin inhibits human endometrial carcinoma proliferation via G0/G1 cell cycle arrest and mitochondrial-dependent

Xiao-Li Li1, Run-Hui Ma2, Zhi-Jing Ni2

  • 1School of Food and Biological Engineering, Hefei University of Technology, Hefei, 230009, People's Republic of China.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|December 28, 2020
PubMed

Insights

Dioscin exhibits anti-cancer properties by inhibiting endometrial cancer cell proliferation and inducing apoptosis through both mitochondrial and death receptor pathways. This natural compound shows promise for endometrial cancer prevention and treatment.

Area of Science:

  • Pharmacology and Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Endometrial cancer remains a significant health concern.
  • Natural compounds are increasingly investigated for therapeutic potential.
  • Dioscin, a saponin, has shown various biological activities.

Purpose of the Study:

  • To investigate the anti-cancer effects of dioscin on human endometrial cancer Ishikawa cells.
  • To elucidate the molecular mechanisms underlying dioscin's action.
  • To assess dioscin's potential in endometrial cancer prevention and treatment.

Main Methods:

  • Cell proliferation assays to determine the half-maximal inhibitory concentration (IC50).
  • Cell cycle analysis to identify cell cycle arrest.
  • Apoptosis assays including mitochondrial pathway and death receptor pathway analysis.
  • Western blotting to assess protein expression levels.

Main Results:

  • Dioscin significantly suppressed Ishikawa cell proliferation with an IC50 of 2.37 μM.
  • Dioscin induced G0/G1 cell cycle arrest by up-regulating p16, p21, p27 and down-regulating Cyclin A/D/E, CDK2/4/6.
  • Dioscin promoted apoptosis via the mitochondrial pathway (Bcl family proteins, ROS, Caspase 9/3, mitochondrial membrane permeability) and the death receptor pathway (Fas, TNF-R1, Caspase 8).

Conclusions:

  • Dioscin demonstrates significant anti-cancer effects against human endometrial cancer cells.
  • Dioscin induces apoptosis through both intrinsic (mitochondrial) and extrinsic (death receptor) pathways.
  • Dioscin holds potential as a therapeutic agent for endometrial cancer prevention and treatment.
Keywords:
ApoptosisCell cycleDioscinIshikawaMitochondrial pathway

More Related Videos

Two Methods for Establishing Primary Human Endometrial Stromal Cells from Hysterectomy Specimens09:15

Two Methods for Establishing Primary Human Endometrial Stromal Cells from Hysterectomy Specimens

Published on: May 23, 2014

23.3K
Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization14:55

Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization

Published on: September 1, 2018

10.8K

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...
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.
37.5K
Molecular Factors Affecting Cell Division01:27

Molecular Factors Affecting Cell Division

Several external and internal factors influence the initiation and inhibition of cell division. For instance, the death of nearby cells or the release of human growth hormone (hGH) promotes cell division. In contrast, lack of hGH or crowding of cells can inhibit cell division.
Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...
3.6K
The Cell Cycle Control System01:28

The Cell Cycle Control System

The cell cycle regulation directs how a cell proceeds from one phase to the next and begins mitosis. The cell cycle control system includes intracellular regulatory molecules and external triggers. They provide "stop" or "advance" signals and operate at specific cell cycle stages termed checkpoints to ensure that a particular process is completed before the cell advances to the next phase.
Cyclins and cyclin-dependent kinases (Cdks) are the primary cell cycle regulators and...
4.6K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
7.4K
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...
7.5K