Related Experiment Video

Updated: Mar 15, 2026

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
10:43

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids

Published on: December 23, 2022

4.2K

ATF3 suppresses ESCC via downregulation of ID1

Jian Li1, Zishan Yang2, Zhiuguo Chen3

  • 1Department of Gastroenterology, People's Hospital of Zhengzhou University, Henan Provincial People's Hospital, Zhengzhou, Henan 450052, P.R. China.

Oncology Letters
|September 8, 2016
PubMed

Insights

Activating transcription factor 3 (ATF3) is reduced in esophageal cancer, while inhibitor of DNA binding 1 (ID1) is increased. Restoring ATF3 inhibits cancer cell proliferation and metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Esophageal cancer has a high mortality rate due to early metastasis.
  • Mechanisms of esophageal cancer progression are not fully understood.

Purpose of the Study:

  • To investigate the role of activating transcription factor 3 (ATF3) in esophageal squamous cell carcinoma (ESCC).
  • To explore the relationship between ATF3 and inhibitor of DNA binding 1 (ID1) in ESCC.

Main Methods:

  • Immunohistochemical analysis of ESCC tissues.
  • Transfection of ESCC cell lines with ATF3-overexpression plasmid.
  • Assessment of cell proliferation, motility, migration, E-cadherin, cyclin D1, and Twist expression.

Main Results:

  • ATF3 expression was reduced, while ID1 was overexpressed in ESCC tissues, showing an inverse correlation.
  • Overexpression of ATF3 inhibited ESCC cell proliferation, motility, and migration.
  • ATF3 overexpression led to increased E-cadherin and decreased cyclin D1 and Twist expression.
  • An inverse regulatory interaction was observed between ATF3 and ID1.

Conclusions:

  • ATF3 exhibits tumor suppressive features in esophageal cancer.
  • ATF3 inhibits cancer metastasis through a novel mechanism involving regulation of ID1, E-cadherin, cyclin D1, and Twist.
Keywords:
activating transcription factor 3esophageal squamous cell carcinomainhibitor of DNA binding 1metastasisproliferation

More Related Videos

Development of Compendium for Esophageal Squamous Cell Carcinoma03:36

Development of Compendium for Esophageal Squamous Cell Carcinoma

Published on: April 12, 2024

898
Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter11:32

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

7.5K

Related Concept Videos

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
63
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...
5.4K
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...
2.6K
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...
6.2K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.9K