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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 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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Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

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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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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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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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Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

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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. 
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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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Mitochondrial apoptosis: killing cancer using the enemy within.

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Cancer cells evade programmed cell death (apoptosis) to grow and spread. This review explores how blocking mitochondrial apoptosis contributes to cancer and discusses new therapies targeting this pathway.

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Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Medicine

Background:

  • Apoptotic cell death is a crucial mechanism that suppresses cancer development and progression.
  • Inhibition of apoptosis is a hallmark of cancer, enabling tumor growth, transformation, and metastasis.
  • Apoptosis is also a key mechanism of action for many cancer therapies.

Purpose of the Study:

  • To review the critical role of apoptosis in cancer development and treatment.
  • To focus on the mitochondrial pathway of apoptosis, a frequently dysregulated process in cancer.
  • To discuss novel therapeutic strategies aimed at inducing mitochondrial apoptosis in cancer cells.

Main Methods:

  • Review of existing literature on apoptosis, cancer biology, and therapeutic strategies.
  • Detailed examination of the mitochondrial pathway of apoptosis and its regulation by BCL-2 family proteins.
  • Analysis of mechanisms by which cancer cells evade apoptosis and potential therapeutic interventions.

Main Results:

  • Mitochondrial outer membrane permeabilization (MOMP) is the critical event in the mitochondrial apoptosis pathway.
  • Cancer cells frequently deregulate the mitochondrial pathway to survive and proliferate.
  • The BCL-2 protein family plays a central role in regulating MOMP.
  • Various strategies are being developed to specifically induce mitochondrial apoptosis in cancer cells.

Conclusions:

  • Targeting the mitochondrial apoptosis pathway holds significant therapeutic promise for cancer treatment.
  • Understanding the regulation of MOMP by BCL-2 proteins is key to developing effective cancer therapies.
  • New approaches to induce mitochondrial apoptosis offer potential for overcoming therapeutic resistance in cancer.