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Related Concept Videos

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 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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Autophagic Cell Death01:18

Autophagic Cell Death

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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
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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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Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Overview of Cell Death01:30

Overview of Cell Death

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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.
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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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Apoptosis - Fueling the oncogenic fire.

Camila Castillo Ferrer1,2, Kevin Berthenet3,4, Gabriel Ichim3,4

  • 1Cancer Target and Experimental Therapeutics, Institute for Advanced Biosciences, INSERM U1209, CNRS UMR5309, Grenoble Alpes University, France.

The FEBS Journal
|November 12, 2020
PubMed
Summary

Programmed cell death, or apoptosis, typically suppresses tumors. However, cancer cells can hijack apoptosis to promote tumor growth and metastasis through complex interactions and effector roles.

Keywords:
apoptosiscancercaspasesmitochondriaoncogenesis

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

  • Cell biology
  • Cancer research
  • Molecular oncology

Background:

  • Apoptosis is a fundamental process for maintaining organismal health and is traditionally viewed as a tumor suppressor mechanism.
  • Recent evidence suggests that apoptosis can paradoxically promote tumor progression and metastasis through noncanonical functions.
  • Cancer cells may exploit apoptosis at various levels, including microenvironmental interactions and the pro-oncogenic roles of apoptosis effectors like caspases and mitochondria.

Purpose of the Study:

  • To review and highlight recently identified mechanisms by which apoptosis and its effectors contribute to cancer aggressiveness.
  • To underscore the importance of understanding the noncanonical roles of apoptosis in cancer biology.
  • To emphasize the potential of targeting these noncanonical pathways for improved cancer therapies.

Main Methods:

  • This is a review article, synthesizing findings from existing research.
  • Literature search and critical analysis of studies on apoptosis and cancer.
  • Focus on mechanisms involving apoptotic cells, caspases, and mitochondria in cancer progression.

Main Results:

  • Apoptosis, while a cell death pathway, can be co-opted by cancer cells to enhance tumor growth and spread.
  • Noncanonical functions of apoptosis, including interactions with the tumor microenvironment, can promote malignancy.
  • Dysfunctional roles of caspases and mitochondria during failed apoptosis can contribute to cancer aggressiveness.

Conclusions:

  • A deeper understanding of how apoptosis and its effectors promote cancer is critical.
  • Targeting the noncanonical roles of apoptosis may offer novel therapeutic strategies for cancer treatment.
  • Further research into these pro-tumorigenic aspects of apoptosis is essential for advancing cancer therapy.