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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...
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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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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Apoptotic signaling by c-MYC.

B Hoffman1, D A Liebermann

  • 1Department of Biochemistry, Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA 19140, USA. pboya@cib.csic.es

Oncogene
|October 29, 2008
PubMed
Summary
This summary is machine-generated.

The oncogene c-MYC (myelocytomatosis oncogene) drives cell growth and can trigger apoptosis. This review explores how c-MYC interacts with cell survival pathways and the tumor suppressor p53 to influence cell death and cancer progression.

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Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cellular Signaling

Background:

  • The c-MYC oncogene plays a critical role in regulating cell growth, differentiation, and apoptosis.
  • Abnormal c-MYC expression is a hallmark of numerous human cancers.
  • Understanding c-MYC's role in apoptosis is crucial for cancer research and treatment strategies.

Purpose of the Study:

  • To provide an overview of c-MYC's function in apoptosis.
  • To elucidate the interplay between c-MYC, p53, and apoptotic pathways.
  • To present a model for c-MYC's role in myeloid differentiation and cancer.

Main Methods:

  • Literature review and synthesis of existing research on c-MYC and apoptosis.
  • Analysis of c-MYC's interaction with intrinsic (mitochondrial) and extrinsic (death receptor) apoptotic pathways.
  • Integration of c-MYC's role with the tumor suppressor p53.

Main Results:

  • c-MYC overexpression sensitizes cells to apoptosis through various stimuli.
  • c-MYC amplifies the mitochondrial apoptotic pathway and influences death receptor signaling.
  • The tumor suppressor p53 is a key mediator in c-MYC-induced apoptosis.

Conclusions:

  • c-MYC's apoptotic function is context-dependent, varying with cell type and physiological state.
  • Deregulated c-MYC can prematurely induce apoptosis during differentiation while simultaneously inhibiting the differentiation process.
  • Targeting c-MYC-mediated apoptosis offers potential therapeutic strategies for cancer.