Related Experiment Video

Updated: Aug 30, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Apoptotic pathways of epothilone BMS 310705

Denise Uyar1, Nagio Takigawa, Tarek Mekhail

  • 1The Cleveland Clinic Foundation, Experimental Therapeutics Program, Taussig Cancer Center/R40, 9500 Euclid Avenue, Cleveland, OH 44195, USA. uyard@ccf.org

Gynecologic Oncology
|October 8, 2003
PubMed
Abstract

Insights

BMS 310705, a novel epothilone B analog, effectively induces apoptosis and reduces cancer cell survival. It activates the mitochondrial pathway, showing promise in preclinical models resistant to standard therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • BMS 310705 is a novel, water-soluble epothilone B analog.
  • Currently undergoing Phase I clinical trials for various malignancies.
  • Investigated in a cell culture model resistant to platinum/paclitaxel therapy.

Purpose of the Study:

  • To evaluate the apoptosis pathway induced by BMS 310705.
  • To assess the efficacy of BMS 310705 in a platinum/paclitaxel-refractory cancer model.

Main Methods:

  • Cell culture treated with BMS 310705.
  • Apoptosis, cell survival, and caspase activity assays (caspase-3, -8, -9).
  • Mitochondrial cytochrome c release analysis.

Main Results:

  • BMS 310705 induced apoptosis in >25% of cells within 24 hours.
  • Significantly reduced cell survival compared to paclitaxel (P < 0.02).
  • Increased caspase-9 and -3 activity, with cytochrome c release at 12 hours, indicating mitochondrial pathway activation.

Conclusions:

  • BMS 310705 effectively induces apoptosis and decreases survival in the tested model.
  • The drug utilizes the mitochondrial-mediated pathway for apoptosis.
  • Demonstrates potential against malignancies refractory to conventional chemotherapy.

More Related Videos

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

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...
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...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
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...
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...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.