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Related Concept Videos

Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

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.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
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Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

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 goblet,...
Cellular Adaptation IV: Dysplasia and Metaplasia01:24

Cellular Adaptation IV: Dysplasia and Metaplasia

DysplasiaDysplasia refers to abnormal changes in the size, shape, and organization of mature cells, characterized by pleomorphism, nuclear abnormalities, and increased mitotic activity. It commonly affects epithelial tissues, including the cervix, gastrointestinal tract, respiratory mucosa, and endometrium. Although it may occur alongside hyperplasia, dysplasia is not a true adaptive response but a preneoplastic change with potential to progress to cancer.When confined above the basement...
Abnormal Proliferation02:23

Abnormal Proliferation

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 daughter...
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Related Experiment Video

Updated: Jul 16, 2026

In vitro Organoid Culture of Primary Mouse Colon Tumors
07:33

In vitro Organoid Culture of Primary Mouse Colon Tumors

Published on: May 17, 2013

The STAT3-CCND2 Axis Drives a Proliferative Metaplastic Precursor Population in Gastric Intestinal Metaplasia.

Fazhan Li1,2, Huijuan Wen1,2, Feifei Ren1,2

  • 1Henan Key Laboratory for Helicobacter Pylori and Digestive Tract Microecology, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan, China.

Journal of Cellular and Molecular Medicine
|July 15, 2026
PubMed
Summary

STAT3 and CCND2 are key drivers of early gastric intestinal metaplasia (GIM), a precancerous lesion. Targeting this STAT3-CCND2 axis may enable early detection and prevention of gastric cancer.

Keywords:
DNA methylationgastric intestinal metaplasiagastric organoidssingle‐cell RNA sequencingtranscriptomic sequencing

Related Experiment Videos

Last Updated: Jul 16, 2026

In vitro Organoid Culture of Primary Mouse Colon Tumors
07:33

In vitro Organoid Culture of Primary Mouse Colon Tumors

Published on: May 17, 2013

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Oncology

Background:

  • Gastric intestinal metaplasia (GIM) is a critical precancerous lesion.
  • Drivers of GIM's early proliferation and reprogramming are not well-defined.
  • Identifying GIM regulators is essential for gastric cancer interception.

Purpose of the Study:

  • To identify key regulators of early gastric intestinal metaplasia (GIM).
  • To elucidate the role of STAT3 and CCND2 in GIM pathogenesis.
  • To explore potential therapeutic targets for gastric cancer prevention.

Main Methods:

  • Integrated epigenomic-transcriptomic analysis of human GIM and normal tissues.
  • Single-cell RNA sequencing of patient-derived gastric organoids.
  • Functional validation using STAT3 knockdown in GIM organoids (qRT-PCR, immunofluorescence, dual-luciferase assay).

Main Results:

  • STAT3 identified as a top regulator of hypomethylated, upregulated genes in GIM.
  • STAT3 directly transactivates CCND2.
  • A proliferative GIM-precursor cell population co-expressing STAT3 and CCND2 was identified.
  • STAT3 knockdown reduced CCND2 and intestinal markers (CDX2, MUC2) in GIM organoids.

Conclusions:

  • The STAT3-CCND2 axis is central to early gastric intestinal metaplasia pathogenesis.
  • This axis represents a promising target for early detection and chemoprevention of gastric cancer.