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Related Concept Videos

Renewal of Intestinal Stem Cells01:23

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The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
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Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Adult Stem Cells01:33

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Stem cells are undifferentiated cells that divide and produce more stem cells or progenitor cells that differentiate into mature, specialized cell types. All the cells in the body are generated from stem cells in the early embryo, but small populations of stem cells are also present in many adult tissues including the bone marrow, brain, skin, and gut. These adult stem cells typically produce the various cell types found in that tissue—to replace cells that are damaged or to continuously...
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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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Epigenetic Gatekeeping of Intestinal Stem Cell Transformation.

Alireza Lorzadeh1, Sweta Sharma1, Geroge Ye1

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Epigenetic marks, specifically H3K27me3, act as a barrier against intestinal tumors by maintaining stem cell properties. Loss of this mark in cancer cells allows fetal gene reactivation and tumor growth, explaining treatment resistance.

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Area of Science:

  • Epigenetics
  • Molecular Biology
  • Cancer Biology

Background:

  • Adult intestinal stem cells retain limited cell plasticity, contributing to tumor initiation and relapse.
  • Epigenetic mechanisms maintaining stemness and restricting fetal gene expression in adults, and their loss in tumors, remain unclear.
  • Tumorigenesis involves non-stem cells potentially replenishing cancer stem cells after targeted therapies.

Purpose of the Study:

  • Investigate the epigenetic features governing reversible stemness in adult intestinal crypt cells.
  • Determine the role of H3K27ac and H3K27me3 in maintaining stem-cell properties and restricting fetal gene expression.
  • Elucidate how epigenetic rewiring, including H3K27me3 loss, contributes to intestinal tumorigenesis and therapy resistance.

Main Methods:

  • Analysis of H3K27ac and H3K27me3 marks at enhancers in normal and tumor intestinal cells.
  • Utilizing *Apc-/-* mouse models with constitutive Wnt activity to study tumorigenesis.
  • Investigating the impact of accelerated or preserved H3K27me3 loss on stemness-related enhancers and tumor progression.
  • Examining DNA demethylation at superenhancer domains in tumor growth.

Main Results:

  • Reversible stemness in normal adult intestinal cells depends on a balance between H3K27ac and H3K27me3 marks.
  • Loss of H3K27me3 at enhancers transforms intestinal stem cells, reactivates fetal genes, and promotes tumor growth.
  • H3K27me3 loss erases distinctions between stem and non-stem cells, conferring stemness and contributing to therapy resistance.
  • Human colorectal cancers exhibit similar epigenetic rewiring, with H3K27me3 loss correlating with tumor progression.

Conclusions:

  • H3K27me3 at Wnt-responsive enhancers is a critical barrier to intestinal tumorigenesis.
  • Aberrant reactivation of hundreds of fetal genes is driven by H3K27me3 loss during transformation.
  • Understanding this epigenetic regulation offers insights into cancer stem cell targeting and therapeutic resistance.