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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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...
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Electron Transport Chain: Complex I and II01:46

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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
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Apoptosis01:30

Apoptosis

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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...
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The Extrinsic Apoptotic Pathway01:17

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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...
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Caspases01:24

Caspases

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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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Related Experiment Video

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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
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13-Oxyingenol dodecanoate, a cytotoxic ingenol derivative, induces mitochondrial apoptosis and caspase-dependent Akt

Ming Liu1, Weiyi Zhang1, Genzhu Wang1

  • 1Key Laboratory of Marine Drugs, Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, Qingdao, 266003, China.

Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine
|November 30, 2015
PubMed
Summary

13-Oxyingenol dodecanoate (13OD), derived from traditional medicine, shows potent cytotoxicity against chronic myeloid leukemia K562 cells. This ingenol derivative induces apoptosis through novel mechanisms, suggesting its potential for anticancer drug development.

Keywords:
13-Oxyingenol dodecanoateAktApoptosisEuphorbia kansuimTOR

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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
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Area of Science:

  • Pharmacology
  • Oncology
  • Natural Products Chemistry

Background:

  • 13-Oxyingenol dodecanoate (13OD) is an ingenol derivative from Euphorbia kansui.
  • Its bioactivity has not been previously reported.

Purpose of the Study:

  • To investigate the bioactivity of 13OD.
  • To explore its cytotoxic effects on chronic myeloid leukemia (CML) K562 cells.
  • To elucidate the underlying molecular mechanisms of its action.

Main Methods:

  • In vitro cytotoxicity assays using K562 cells.
  • Cell cycle analysis (G2/M phase arrest).
  • Apoptosis assays, including mitochondrial membrane potential and reactive oxygen species (ROS) level determination.
  • Western blot analysis to assess protein levels (Akt, ERK) and caspase-dependent pathways.

Main Results:

  • 13OD demonstrated potent cytotoxicity against K562 cells.
  • It inhibited cell proliferation and induced G2/M phase arrest.
  • 13OD triggered apoptosis by disrupting mitochondrial membrane potential and increasing ROS levels.
  • Mechanistically, 13OD decreased Akt protein via caspase-dependent pathways and activated ERK, which conferred a protective role.

Conclusions:

  • 13OD exhibits significant cytotoxic and pro-apoptotic effects on K562 cells through novel mechanisms.
  • The findings suggest 13OD as a potential lead compound for developing new anticancer agents.
  • Further research into 13OD could advance rational drug design for leukemia treatment.