Related Experiment Video

Updated: May 13, 2026

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

Dachshund binds p53 to block the growth of lung adenocarcinoma cells

Ke Chen1, Kongming Wu, Shaoxin Cai

  • 1Departments of Cancer Biology, Stem Cell Biology and Regenerative Medicine, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia,PA 19107, USA.

Cancer Research
|March 16, 2013
PubMed

Insights

DACH1 protein suppresses non-small cell lung cancer (NSCLC) growth by binding to p53. Reduced DACH1 expression correlates with NSCLC progression, highlighting DACH1 as a potential therapeutic target for lung cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Non-small cell lung cancer (NSCLC) is a leading cause of cancer mortality worldwide.
  • Hyperactive epidermal growth factor receptor (EGFR) and mutant p53 are key drivers of NSCLC progression.
  • The Drosophila gene Dachshund (Dac) is known to inhibit hyperactive EGFR.

Purpose of the Study:

  • To investigate the role of DACH1 expression in the development of NSCLC.
  • To determine the mechanism by which DACH1 influences NSCLC growth and progression.

Main Methods:

  • Analysis of DACH1 protein and mRNA expression in human NSCLC tissues.
  • In vivo studies involving re-expression of DACH1 in NSCLC models.
  • Chromatin immunoprecipitation sequencing (ChIP-seq) to identify p53-bound genes.
  • Assessment of SOX2 expression in relation to DACH1 levels.

Main Results:

  • DACH1 expression was found to be reduced in human NSCLC.
  • Re-expression of DACH1 inhibited NSCLC colony formation and tumor growth, mediated by p53.
  • DACH1 directly binds to p53, influencing cell-cycle arrest and inhibiting colony formation.
  • DACH1 represses SOX2 expression, a stem cell factor, which is inversely correlated with DACH1 in NSCLC.

Conclusions:

  • DACH1 acts as a tumor suppressor in NSCLC by interacting with p53.
  • DACH1-p53 binding inhibits NSCLC cellular growth and proliferation.
  • DACH1 may serve as a potential therapeutic target for NSCLC treatment.

More Related Videos

Yeast As a Chassis for Developing Functional Assays to Study Human P5314:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Related Concept Videos

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...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...