ArticleGenes & cancer2014
Impairement of HT29 Cancer Cells Cohesion by the Soluble Form of Neurotensin Receptor-3.
Article in Genes & cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- SORT1 promote the metastasis and invasion of hepatocellular carcinoma via p38/β-catenin/ZEB1 signaling pathway.Cell death & disease · 2025Article
- Bradykinin and Neurotensin Analogues as Potential Compounds in Colon Cancer Therapy.International journal of molecular sciences · 2023Article
- Deciphering Mechanisms of Action of Sortilin/Neurotensin Receptor-3 in the Proliferation Regulation of Colorectal and Other Cancers.International journal of molecular sciences · 2022Review
- The Neuropeptide System and Colorectal Cancer Liver Metastases: Mechanisms and Management.International journal of molecular sciences · 2020Review
- Dimerization of sortilin regulates its trafficking to extracellular vesicles.The Journal of biological chemistry · 2018Article
- Review
- Sortilin limits EGFR signaling by promoting its internalization in lung cancer.Nature communications · 2017Article
- Focal Adhesion Kinase-Dependent Role of the Soluble Form of Neurotensin Receptor-3/Sortilin in Colorectal Cancer Cell Dissociation.International journal of molecular sciences · 2016Review
- p75 neurotrophin receptor and pro-BDNF promote cell survival and migration in clear cell renal cell carcinoma.Oncotarget · 2016Article
- Sortilin is associated with breast cancer aggressiveness and contributes to tumor cell adhesion and invasion.Oncotarget · 2015Article
- Targeting two-pore domain K(+) channels TREK-1 and TASK-3 for the treatment of depression: a new therapeutic concept.British journal of pharmacology · 2015Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neurotensin (NT) receptor-3 (NTSR3), also called sortilin is a multifunctional protein localized at the intracellular and plasma membrane level. The extracellular domain of NTSR3 (sNTSR3) is released by shedding from several cell lines including colonic cancer cells. This soluble protein acts as an active ligand through its ability to bind, to be internalized in the human adenocarcinoma epithelial HT29 cells and to stimulate the PI3 kinase pathway. The aim of this study was to investigate cellular responses induced by sNTSR3 in HT29 cells. The cellular functions of sNTSR3 were monitored by immunofluocytochemistry, electron microscopy and quantitative PCR in order to characterize the cell shape and the expression of adhesion proteins. We evidenced that sNTSR3 significantly regulates the cellular morphology as well as the cell-cell and the cell-matrix adherens properties by decreasing the expession of several integrins and by modifying the structure of desmosomes. Altogether, these properties lead to an increase of cell detachment upon sNTSR3 treatment on HT29, HCT116 and SW620 cancer cells. Our results indicate that sNTSR3 may induce the first phase of a process which weaken HT29 epithelial properties including desmosome architecture, cell spreading, and initiation of cell separation, all events which could be responsible for cancer metastasis.
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