Related Experiment Video

Updated: Apr 28, 2026

Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling
09:33

Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling

Published on: March 20, 2018

13.4K

Ellipticine induces apoptosis in T-cell lymphoma via oxidative DNA damage

Cecilia Savorani1, Valentina Manfé, Edyta Biskup

  • 1Department of Dermatology, Bispebjerg Hospital , Copenhagen , Denmark.

Leukemia & Lymphoma
|June 6, 2014
PubMed

Insights

Ellipticine induces cancer cell death in cutaneous T-cell lymphoma (CTCL) by causing DNA damage, not by reactivating the p53 protein. This finding offers a new therapeutic strategy for chemoresistant CTCL.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • The tumor suppressor p53 is frequently mutated in human cancers, making its restoration a key therapeutic strategy.
  • Cutaneous T-cell lymphoma (CTCL) is a progressive, chemoresistant cancer with limited treatment options.
  • Ellipticine is being investigated as a p53 reactivator for cancer treatment.

Purpose of the Study:

  • To investigate the mechanism of ellipticine's antitumor activity in CTCL.
  • To determine if ellipticine's efficacy relies on p53 reactivation in CTCL models.
  • To explore the role of DNA damage in ellipticine-induced apoptosis.

Main Methods:

  • Testing ellipticine in three CTCL cell lines with varying p53 statuses (wild-type, mutated, and null).
  • Utilizing p53 siRNA knockdown to assess p53's requirement for ellipticine's effects.
  • Employing α-tocopherol (an antioxidant) to investigate the role of oxidative stress and DNA damage.

Main Results:

  • Ellipticine induced apoptosis in CTCL cell lines with wild-type and mutated p53.
  • p53 was not required for ellipticine-induced apoptosis, even in cell lines with mutated p53.
  • Apoptosis induced by ellipticine was inhibited by α-tocopherol, indicating a link to oxidative DNA damage.

Conclusions:

  • Ellipticine triggers apoptosis in CTCL cells primarily through inducing DNA damage.
  • The anti-CTCL effect of ellipticine does not depend on p53 activation.
  • Ellipticine represents a potential therapeutic agent for CTCL, acting via a p53-independent DNA damage pathway.
Keywords:
DNA damageEllipticineapoptosiscutaneous T-cell lymphomap53

More Related Videos

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

10.8K
Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors04:36

Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors

Published on: October 17, 2025

1.1K

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...
6.2K
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...
87
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...
6.2K
Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
31.2K
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
4.6K
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...
8.5K