Related Experiment Video

Updated: Aug 17, 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

Role of early plasma membrane events in chemotherapy-induced cell death

Marie-Thérèse Dimanche-Boitrel1, Olivier Meurette, Amélie Rebillard

  • 1INSERM U620, Faculty of Pharmacy, Université Rennes 1, 2 Av du Pr Léon Bernard, 35043 Rennes, France. marie-therese.boitrel@rennes.inserm.fr

Drug Resistance Updates : Reviews and Commentaries in Antimicrobial and Anticancer Chemotherapy
|June 9, 2005
PubMed

Insights

Chemotherapy can trigger cancer cell death through plasma membrane lipid rafts and the Fas death pathway. This review explores early membrane events, including fluidity changes and acid sphingomyelinase activation, in chemotherapy-induced apoptosis.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Current anticancer therapies primarily induce apoptosis, a programmed cell death pathway.
  • The precise molecular mechanisms underlying chemotherapy-induced apoptosis are not fully elucidated.
  • DNA-damaging agents and other antitumor drugs can initiate apoptosis through novel pathways.

Purpose of the Study:

  • To review the role of early plasma membrane events in chemotherapy-induced cell death.
  • To highlight the involvement of plasma membrane lipid rafts and the death receptor pathway.
  • To explore the interrelationships between plasma membrane changes and apoptosis induction.

Main Methods:

  • Literature review focusing on chemotherapy mechanisms.
  • Analysis of studies investigating plasma membrane alterations.
  • Examination of signaling pathways involved in chemotherapy response.

Main Results:

  • Chemotherapy agents can induce apoptosis via signaling through plasma membrane lipid rafts.
  • Early plasma membrane events, including altered fluidity and acid sphingomyelinase activation, are critical.
  • The Fas death pathway is implicated in chemotherapy-induced cell death signaling.

Conclusions:

  • Plasma membrane dynamics play a crucial role in mediating chemotherapy's cytotoxic effects.
  • Targeting early plasma membrane events may offer novel therapeutic strategies.
  • Understanding these pathways is essential for optimizing anticancer treatments.

More Related Videos

Assessing Cell Viability and Death in 3D Spheroid Cultures of Cancer Cells10:33

Assessing Cell Viability and Death in 3D Spheroid Cultures of Cancer Cells

Published on: June 16, 2019

Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
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...
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...
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...
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...
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...