Related Experiment Video

Updated: Jun 27, 2026

Tropomodulin 3 Overexpression as a Marker for Platinum Resistance and Immune Infiltration in Ovarian Cancer
09:40

Tropomodulin 3 Overexpression as a Marker for Platinum Resistance and Immune Infiltration in Ovarian Cancer

Published on: August 2, 2024

Enhanced complement resistance in drug-selected P-glycoprotein expressing multi-drug-resistant ovarian carcinoma

K E Odening1, W Li, R Rutz

  • 1Department of Internal Medicine III, Cardiology, University of Freiburg, Freiburg, Germany.

Clinical and Experimental Immunology
|December 2, 2008
PubMed

Insights

Multi-drug resistance (MDR) in ovarian cancer cells increases resistance to complement-dependent cytotoxicity (CDC). This resistance is linked to membrane-bound complement regulatory proteins (mCRP), not P-glycoprotein (P-gp).

Area of Science:

  • Oncology
  • Immunology
  • Pharmacology

Background:

  • Multi-drug resistance (MDR) is a significant challenge in cancer chemotherapy.
  • The relationship between P-glycoprotein (P-gp) expression and complement-dependent cytotoxicity (CDC) susceptibility is unclear.
  • Ovarian carcinoma cells and their MDR variants were studied for complement sensitivity.

Purpose of the Study:

  • To investigate the role of P-glycoprotein (P-gp) and membrane-bound complement regulatory proteins (mCRP) in chemoresistant ovarian cancer cell sensitivity to complement-dependent cytotoxicity (CDC).

Main Methods:

  • Compared CDC susceptibility in chemo-selected MDR ovarian carcinoma cells versus their sensitive counterparts.
  • Analyzed expression of P-gp, membrane-bound complement regulatory proteins (mCRP), and soluble complement inhibitors.
  • Investigated the impact of MDR1 gene transfection and chemotherapeutic treatment on CDC resistance.
  • Utilized blocking agents for P-gp and mCRP functions.

Main Results:

  • Chemoselected MDR cells exhibited increased resistance to CDC, correlated with higher mCRP and soluble inhibitor levels.
  • MDR1 gene transfection alone did not affect CDC susceptibility.
  • Subsequent chemotherapy in transfected cells increased complement resistance, associated with elevated mCRP.
  • Blocking P-gp had no effect on complement resistance, while blocking mCRP enhanced CDC susceptibility.

Conclusions:

  • P-glycoprotein (P-gp) does not confer enhanced resistance to complement-dependent cytotoxicity (CDC) in chemoresistant ovarian cancer cells.
  • Overexpression of membrane-bound complement regulatory proteins (mCRP) plays a significant role in the observed CDC resistance.
  • Chemotherapeutic agents likely induce mCRP overexpression, contributing to complement resistance in MDR ovarian cancer.

More Related Videos

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

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

Related Concept Videos

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...
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...
Treatment Resistent Cancers02:56

Treatment Resistent 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...
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...