Related Experiment Video

Updated: May 8, 2026

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells
15:53

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

Gemcitabine eliminates double minute chromosomes from human ovarian cancer cells

Lisa Yu1, Yan Zhao, Chao Quan

  • 1Laboratory of Medical Genetics, Harbin Medical University, Harbin, China.

Plos One
|August 31, 2013
PubMed

Insights

The cancer drug gemcitabine effectively reduces double minute chromosomes (DMCs) in ovarian cancer cells. This reduction, even at low concentrations, inhibits cancer progression and drug resistance by decreasing amplified oncogenes.

Area of Science:

  • Cytogenetics
  • Cancer Biology
  • Pharmacology

Background:

  • Double minute chromosomes (DMCs) are hallmarks of gene amplification in cancer cells.
  • Amplified genes on DMCs, including oncogenes and drug resistance genes, drive cancer progression and treatment resistance.
  • Eliminating DMCs is a potential strategy to reduce cancer malignancy.

Purpose of the Study:

  • To investigate the effectiveness of gemcitabine in causing the loss of DMCs from ovarian cancer cells.
  • To compare gemcitabine's efficacy with hydroxyurea in reducing DMCs.
  • To explore the impact of gemcitabine-induced DMC loss on cancer cell biology.

Main Methods:

  • Treatment of ovarian cancer cell line UACC-1598 with gemcitabine.
  • Quantification of DMCs and amplified gene levels.
  • Assessment of DNA damage markers (γ-H2AX) and micronuclei formation.
  • Evaluation of cellular functions including growth, colony formation, and invasion.

Main Results:

  • Gemcitabine significantly decreased DMC numbers at much lower concentrations than hydroxyurea.
  • Gemcitabine treatment led to a reduction in amplified genes at the DNA level.
  • Gemcitabine induced DNA damage, evidenced by γ-H2AX signals within micronuclei, correlating with DMC loss.
  • Gemcitabine treatment resulted in decreased ovarian cancer cell growth, colony formation, and invasion.

Conclusions:

  • Gemcitabine is a potent agent for reducing DMCs in ovarian cancer cells.
  • Gemcitabine's ability to decrease DMCs and amplified genes impacts key cancer cell behaviors.
  • These findings highlight gemcitabine's potential as a therapeutic strategy targeting DMCs in ovarian cancer.

More Related Videos

Enrichment for Chemoresistant Ovarian Cancer Stem Cells from Human Cell Lines11:50

Enrichment for Chemoresistant Ovarian Cancer Stem Cells from Human Cell Lines

Published on: September 10, 2014

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

Related Concept Videos

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...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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...