Related Experiment Video

Updated: Jul 10, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
07:50

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer

Published on: September 18, 2020

Metastatic suppressor genes inactivated by aberrant methylation in gastric cancer

Jian-Feng Wang1, Dong-Qiu Dai

  • 1Department of Surgical Oncology, the First Affiliated Hospital, China Medical University, Shenyang 110001, Liaoning Province, China.

World Journal of Gastroenterology
|October 30, 2007
PubMed
Abstract

Insights

Gastric cancer shows distinct DNA methylation patterns between primary tumors and metastatic lymph nodes. The PTPRG gene

Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • Gastric cancer is a significant health concern with complex molecular underpinnings.
  • Differential DNA methylation plays a crucial role in cancer progression and metastasis.
  • Understanding methylation differences between primary tumors and metastatic sites is vital for targeted therapies.

Purpose of the Study:

  • To identify differentially methylated DNA sequences between gastric primary tumors and metastatic lymph nodes.
  • To investigate the methylation status and expression of the PTPRG gene in gastric cancer.
  • To evaluate the effect of a methylation-suppressive agent on gastric cancer cell lines.

Main Methods:

  • Methylated CpG islands amplification (MCA) coupled with representational difference analysis (RDA) for screening.
  • Methylation-specific PCR (MSP) and RT-PCR to assess PTPRG gene methylation and mRNA expression.
  • Treatment of gastric cancer cell lines with 5-aza-2'-deoxycytidine to observe methylation changes.

Main Results:

  • Nineteen differentially methylated sequences were identified, including those in the PTPRG gene promoter region.
  • Significant differences in PTPRG gene methylation and mRNA expression were observed between primary tumors and metastatic lymph nodes.
  • Treatment with 5-aza-2'-deoxycytidine led to demethylation of PTPRG and recovery of its mRNA expression in cell lines.

Conclusions:

  • Distinct DNA methylation profiles exist between primary gastric tumors and metastatic lymph nodes.
  • The PTPRG gene is differentially methylated in gastric cancer, correlating with metastatic potential.
  • Targeting DNA methylation with agents like 5-aza-2'-deoxycytidine can potentially restore PTPRG expression in gastric cancer.

More Related Videos

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors06:07

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors

Published on: August 5, 2022

Related Concept Videos

Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Epigenetic Regulation01:37

Epigenetic Regulation

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.
X-chromosome...
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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...