Related Experiment Video

Updated: Aug 19, 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

Molecular modes of action of cantharidin in tumor cells

Thomas Efferth1, Rolf Rauh, Stefan Kahl

  • 1German Cancer Research Center, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. thomas.efferth@web.de

Biochemical Pharmacology
|February 16, 2005
PubMed

Insights

Cantharidin, a traditional Chinese medicine, induces cancer cell death via DNA damage and apoptosis. DNA repair pathways, particularly base excision repair, play a key role in resistance to this anti-tumor compound.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Cancer chemotherapy faces challenges due to patient toxicity and tumor drug resistance.
  • Traditional Chinese medicine offers a promising source for novel anticancer agents.
  • Cantharidin (CAN), derived from Mylabris, exhibits anti-tumor activity, but its cytotoxic mechanism remains unclear.

Purpose of the Study:

  • To elucidate the cytotoxic mechanism of cantharidin in cancer cells.
  • To investigate the role of DNA damage and repair pathways in cantharidin's anti-cancer effects.
  • To determine the involvement of p53 and oxidative stress in cantharidin-induced apoptosis.

Main Methods:

  • Investigated cantharidin's effect on leukemia cells, including apoptosis induction.
  • Assessed DNA damage (single- and double-strand breaks) caused by cantharidin.
  • Utilized knockout and transfectant cell lines to evaluate the roles of DNA polymerase beta, ERCC1, base excision repair (BER), and nucleotide excision repair (NER).
  • Examined the sensitivity of oxidative stress-resistant cell variants to cantharidin.

Main Results:

  • Cantharidin induces apoptosis in leukemia cells through a p53-dependent pathway.
  • Cantharidin causes both DNA single- and double-strand breaks.
  • Base excision repair (BER), mediated by DNA polymerase beta, is crucial for cell survival after cantharidin treatment, while nucleotide excision repair (NER) is not.
  • Cell variants resistant to oxidative stress also exhibit resistance to cantharidin.

Conclusions:

  • Cantharidin treatment triggers oxidative stress, leading to DNA damage.
  • The DNA damage induced by cantharidin provokes p53-dependent apoptosis.
  • Base excision repair (BER) is a significant determinant of cellular response to cantharidin, highlighting its potential as an anti-cancer agent targeting DNA repair mechanisms.

Related Concept Videos

Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
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...
Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However, invadopodia can...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...