Related Experiment Video

Updated: May 4, 2026

Development of Compendium for Esophageal Squamous Cell Carcinoma
03:36

Development of Compendium for Esophageal Squamous Cell Carcinoma

Published on: April 12, 2024

974

Epigenetic silencing of checkpoint with fork-head associated and ring finger gene expression in esophageal cancer

Yoshihiro Suzuki1, Yohei Miyagi2, Norio Yukawa3

  • 1Department of Surgery, Hiratsuka Kyosai Hospital, Hiratsuka, Kanagawa 254-8502, Japan.

Oncology Letters
|December 19, 2013
PubMed

Insights

Checkpoint with fork-head associated and ring finger (CHFR) gene hypermethylation silences tumor suppressor function in esophageal cancer. This epigenetic silencing is common and linked to reduced CHFR expression, but not overall survival.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Checkpoint with fork-head associated and ring finger (CHFR) is a crucial mitotic checkpoint gene with demonstrated tumor-suppressor functions.
  • Epigenetic alterations, particularly promoter hypermethylation, are recognized mechanisms for silencing tumor suppressor genes.
  • The specific epigenetic regulation of CHFR and its clinical relevance in esophageal cancer remain largely uncharacterized.

Purpose of the Study:

  • To investigate the epigenetic alterations, specifically promoter methylation, of the CHFR gene in esophageal squamous cell carcinoma.
  • To evaluate the correlation between CHFR gene methylation status and its expression levels.
  • To determine the clinical significance of CHFR expression in relation to clinicopathological features and patient survival.

Main Methods:

  • Quantitative analysis of CHFR mRNA expression in 40 esophageal squamous cell carcinoma patient samples.
  • Assessment of CHFR gene promoter methylation status using methylation-specific polymerase chain reaction (MSP) in 29 patients.
  • Statistical analysis to correlate CHFR expression with methylation status, clinicopathological features, and overall survival.

Main Results:

  • Aberrant hypermethylation of the CHFR gene was identified in 13 out of 29 (44.8%) primary esophageal tumors.
  • CHFR expression levels were significantly lower in samples with methylated CHFR compared to unmethylated samples (P=0.014).
  • CHFR expression did not show a significant correlation with patient characteristics or overall survival.

Conclusions:

  • CpG island hypermethylation of the CHFR gene promoter is a frequent epigenetic event in the development of esophageal cancer.
  • This hypermethylation is a key mechanism responsible for the silencing of the CHFR tumor suppressor gene in esophageal cancer patients.
  • While CHFR silencing occurs commonly, it does not appear to be a significant prognostic biomarker for overall survival in this cohort.
Keywords:
checkpoint with fork-head associated and ring fingeresophageal cancermethylation-specific polymerase chain reaction

More Related Videos

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids10:43

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids

Published on: December 23, 2022

3.8K
Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer07:50

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer

Published on: September 18, 2020

7.0K

Related Concept Videos

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...
3.5K
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.
28.7K
Epigenetic Regulation01:46

Epigenetic Regulation

24.1K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
5.1K
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...
1.8K
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

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.
1.8K