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Related Concept Videos

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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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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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Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Related Experiment Video

Updated: Apr 12, 2026

Evaluating the Differentiation Capacity of Mouse Prostate Epithelial Cells Using Organoid Culture
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Apoptotic cell clearance triggers epithelial fate reprogramming during prostate regression.

Adda-Lee Graham-Paquin1,2, Deepak Saini1, Sophie Viala1,2

  • 1Department of Biochemistry McGill University, Montreal, QC, Canada.

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Summary

Prostate regression after androgen deprivation involves epithelial cells engulfing dying neighbors. This efferocytosis drives progenitor cell fate and tissue remodeling, crucial for understanding prostate cancer.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Urology

Background:

  • Androgen deprivation triggers significant prostate tissue remodeling.
  • The mechanisms behind differentiated prostate epithelial cells adopting a progenitor state are not fully understood.

Purpose of the Study:

  • To investigate the role of efferocytosis in prostate regression and progenitor cell fate acquisition.
  • To elucidate the metabolic and epigenetic changes associated with epithelial efferocytosis during tissue remodeling.

Main Methods:

  • Studied prostate regression in vivo and in vitro models.
  • Analyzed epithelial cell phagocytosis of apoptotic neighbors.
  • Assessed metabolic reprogramming via glycolysis and lactate production.
  • Investigated histone lysine-lactylation patterns.
  • Utilized epithelial-specific dominant-negative MFGE8-D89E expression to block efferocytosis.

Main Results:

  • Epithelial cells are the primary phagocytes during prostate regression, clearing apoptotic cells in coordinated waves.
  • Efferocytosis promotes the acquisition of a progenitor-like state in residual luminal epithelial cells.
  • Metabolic reprogramming, including increased aerobic glycolysis and lactate production, accompanies efferocytosis.
  • Histone lysine-lactylation was enhanced at key gene promoters.
  • Blocking efferocytosis impaired prostate regression and progenitor marker induction.

Conclusions:

  • Epithelial efferocytosis is a critical mechanism linking apoptotic cell clearance to epithelial plasticity during prostate remodeling.
  • Efferocytosis acts as a determinant of cell state transitions in the prostate.
  • These findings have implications for castration-resistant prostate cancer and regenerative processes.