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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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Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
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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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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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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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Prom1 function in development, intestinal inflammation, and intestinal tumorigenesis.

Baktiar O Karim1, Ki-Jong Rhee2, Guosheng Liu1

  • 1Department of Molecular and Comparative Pathobiology, The Johns Hopkins University , Baltimore, MD , USA.

Frontiers in Oncology
|December 3, 2014
PubMed
Summary

Prom1 (Prominin-1) is a cancer stem cell marker involved in intestinal regeneration. Its absence increases susceptibility to intestinal tumor formation, suggesting a therapeutic role in gastrointestinal diseases.

Keywords:
Apc Min miceCD133IBDcolitis-associated colon cancerprominin1

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Area of Science:

  • Gastroenterology
  • Cancer Biology
  • Stem Cell Research

Background:

  • Prominin-1 (Prom1/CD133) is a known cancer stem cell marker in various cancers.
  • Its precise function in intestinal regeneration and its role in inflammatory bowel disease (IBD) remain incompletely understood.

Purpose of the Study:

  • To investigate Prom1's role in intestinal regeneration within the context of IBD.
  • To elucidate Prom1's molecular function and its impact on intestinal tumor development.
  • To assess the consequences of Prom1 deficiency on tumor formation in preclinical models.

Main Methods:

  • Utilized animal models to study intestinal regeneration and tumor formation.
  • Examined the effect of Apc mutations on Prom1 expression in intestinal stem cells and adenomas.
  • Assessed tumor susceptibility in Prom1 knockout mice.

Main Results:

  • Apc mutations correlated with increased Prom1 expression in intestinal crypt stem cells and early adenomas.
  • Prom1 knockout mice exhibited heightened susceptibility to intestinal tumor development.
  • These findings highlight Prom1's involvement in maintaining intestinal homeostasis.

Conclusions:

  • Prom1 plays a significant role in regulating intestinal homeostasis and regeneration.
  • Prom1 deficiency exacerbates intestinal tumor formation.
  • Prom1 represents a potential therapeutic target for inflammatory bowel disease, short bowel syndrome, and colorectal cancer.