Armepavine oxalate induces cell death on CCRF-CEM leukemia cell line through an apoptotic pathway

Guey-Mei Jow1, Yang-Chang Wu, Jih-Hwa Guh

  • 1School of Medicine, Fu Jen Catholic University, 510, Chung-Cheng Road, Hsin-Chuang, Taipei, Hsien, 242 Taiwan, ROC. nurs1019@mails.fju.edu.tw

Life Sciences
|May 26, 2004
PubMed

Insights

Armepavine oxalate induces apoptosis in CCRF-CEM cells by decreasing bcl-2 and increasing caspase-3 expression. This study investigates its effects on cell survival and apoptotic markers.

Area of Science:

  • Pharmacology
  • Cell Biology
  • Molecular Biology

Background:

  • Drug-induced cell death is often linked to DNA damage, affecting bcl-2 and caspase-3 expression.
  • Understanding these pathways is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the effects of armepavines and atherosperminine on CCRF-CEM cell survival.
  • To analyze the impact of these compounds on bcl-2 and caspase-3 expression.

Main Methods:

  • MTT assay for cell survival rate.
  • Hoechst 33258 staining for apoptotic morphology.
  • Western blotting for bcl-2 and caspase-3 protein expression.

Main Results:

  • Armepavine oxalate significantly reduced CCRF-CEM cell survival in a dose- and time-dependent manner.
  • Apoptotic features, including DNA laddering and morphological changes, were observed.
  • Armepavine oxalate decreased bcl-2 expression and increased active caspase-3 expression.

Conclusions:

  • Armepavine oxalate induces apoptosis in CCRF-CEM cells.
  • The observed cell death involves the downregulation of bcl-2 and upregulation of caspase-3.
  • These findings suggest armepavine oxalate's potential in cancer therapy by promoting apoptosis.

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...
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...
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.
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...
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.