Related Experiment Video

Updated: Jul 14, 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

[Netrin-1 and its dependence receptors: role in colorectal cancers]

A Bernet1, P Mehlen

  • 1Apoptose, cancer et développement, laboratoire labellisé La Ligue, FRE CNRS, centre Léon-Berard, 28, rue Laennec, 69008 Lyon, France. bernet@biomserv.univ-lyon1.fr

Pathologie-Biologie
|July 12, 2005
PubMed

Insights

Dependence receptors trigger cell death without their ligand. Their loss in cancer offers tumor cells a survival advantage, particularly in colorectal cancers involving netrin-1.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Dependence receptors induce apoptosis when their ligand is absent.
  • Cancer cells often lose dependence receptors, suggesting a survival advantage.
  • Netrin-1 binding dependence receptors are key in nervous system development and cell death.

Purpose of the Study:

  • To review the role of netrin-1 binding dependence receptors.
  • To explore their function in nervous system development and apoptosis.
  • To discuss their involvement in tumorigenesis, focusing on colorectal cancers.

Main Methods:

  • Literature review of dependence receptors and netrin-1.
  • Analysis of their roles in neural development and apoptosis.
  • Examination of their pathological roles in cancer, especially colorectal cancer.

Main Results:

  • Dependence receptors are crucial for survival signaling.
  • Loss of these receptors in tumors promotes cell survival and proliferation.
  • Netrin-1 dependence receptors are implicated in colorectal cancer progression.

Conclusions:

  • Dependence receptors and netrin-1 signaling are critical in cancer biology.
  • Targeting these pathways may offer new therapeutic strategies for colorectal cancer.
  • Further research is needed to fully elucidate their role in tumorigenesis.

More Related Videos

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo08:19

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Published on: July 20, 2019

In Vivo Immunofluorescence Localization for Assessment of Therapeutic and Diagnostic Antibody Biodistribution in Cancer Research08:53

In Vivo Immunofluorescence Localization for Assessment of Therapeutic and Diagnostic Antibody Biodistribution in Cancer Research

Published on: September 16, 2019

Related Concept Videos

Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...
Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
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.
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...