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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
Netrin-1, a missing link between chronic inflammation and tumor progression.
Andrea Paradisi1, Patrick Mehlen
1Apoptosis, Cancer and Development Laboratory--Equipe labellisée La Ligue, CNRS UMR5238, Université de Lyon, Centre Léon Bérard, Lyon.
Cell Cycle (Georgetown, Tex.)
|March 23, 2010
Summary
Netrin-1 promotes colorectal cancer by inhibiting apoptosis via dependence receptors. NFκB activation in inflammatory bowel disease (IBD) upregulates netrin-1, suggesting it as a therapeutic target for inflammation-driven colorectal cancers.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- Netrin-1, a neuronal guidance cue, is implicated in colorectal cancer (CRC) by regulating apoptosis.
- Netrin-1 dependence receptors (DCC, UNC5H) induce apoptosis without ligands, acting as tumor suppressors.
- Tumors evade apoptosis by losing dependence receptors or gaining netrin-1, disrupting cell survival regulation.
Purpose of the Study:
- To investigate the role of netrin-1 and NFκB in colorectal tumorigenesis, particularly in the context of inflammatory bowel diseases (IBD).
- To explore netrin-1 as a potential therapeutic target for inflammation-driven colorectal cancers.
Main Methods:
- Analysis of netrin-1 as a transcriptional target of NFκB.
- Examination of netrin-1 expression in colorectal tumors, including those from IBD patients.
- Correlation of NFκB activation with netrin-1 gain in colorectal cancers.
Main Results:
- Netrin-1 is a direct transcriptional target of NFκB.
- A subset of colorectal tumors exhibits increased netrin-1 expression concurrent with NFκB activation.
- Colorectal cancers in IBD patients show elevated netrin-1 levels, linking inflammation to netrin-1 induction.
Conclusions:
- NFκB-mediated induction of netrin-1 in IBD patients may promote colorectal tumor development and progression.
- Netrin-1 inhibition represents a promising therapeutic strategy for colorectal cancers associated with chronic inflammation.
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