ArticleBMC cancer2011
Survival advantages conferred to colon cancer cells by E-selectin-induced activation of the PI3K-NFκB survival axis downstream of Death receptor-3.
Article in BMC cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Paeoniflorin ameliorates chronic colitis via the DR3 signaling pathway in group 3 innate lymphoid cells.Journal of pharmaceutical analysis · 2024Article
- Machine learning-based identification of proteomic markers in colorectal cancer using UK Biobank data.Frontiers in oncology · 2024Article
- Death receptor 3 is involved in preeclampsia through regulating placental trophoblast cell physiology by inactivating the PI3K/AKT pathway.Immunity, inflammation and disease · 2023Article
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- The clinical impact of glycobiology: targeting selectins, Siglecs and mammalian glycans.Nature reviews. Drug discovery · 2021Review
- Targeting E-selectin to Tackle Cancer Using Uproleselan.Cancers · 2021Review
- M6A "Writer" GeneFrontiers in oncology · 2021Article
- Rare Modifier Variants Alter the Severity of Cardiovascular Disease in Pseudoxanthoma Elasticum: Identification of Novel Candidate Modifier Genes and Disease Pathways Through Mixture of Effects Analysis.Frontiers in cell and developmental biology · 2021Article
- Regulation of Src Family Kinases during Colorectal Cancer Development and Its Clinical Implications.Cancers · 2020Review
- Death-Domain-Receptor 3 Deletion Normalizes Inflammatory Gene Expression and Prevents Ileitis in Experimental Crohn's Disease.Inflammatory bowel diseases · 2019Article
- Review
- The Tumor Necrosis Factor Family: Family Conventions and Private Idiosyncrasies.Cold Spring Harbor perspectives in biology · 2018Review
- The p38 pathway, a major pleiotropic cascade that transduces stress and metastatic signals in endothelial cells.Oncotarget · 2017Review
- MPA Modulates Tight Junctions' Permeability via Midkine/PI3K Pathway in Caco-2 Cells: A Possible Mechanism of Leak-Flux Diarrhea in Organ Transplanted Patients.Frontiers in physiology · 2017Article
- Diet-induced weight loss leads to a switch in gene regulatory network control in the rectal mucosa.Genomics · 2016Article
- Circulatory shear flow alters the viability and proliferation of circulating colon cancer cells.Scientific reports · 2016Article
- Computational Reconstruction of NFκB Pathway Interaction Mechanisms during Prostate Cancer.PLoS computational biology · 2016Article
- HIV-1 increases TLR responses in human primary astrocytes.Scientific reports · 2015Article
- EGF-induced dynamics of NF-κB and F-actin in A431 cells spread on fibronectin.Histochemistry and cell biology · 2015Article
- Tumor-Associated Endothelial Cells Promote Tumor Metastasis by Chaperoning Circulating Tumor Cells and Protecting Them from Anoikis.PloS one · 2015Article
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundExtravasation of circulating cancer cells is a key event of metastatic dissemination that is initiated by the adhesion of cancer cells to endothelial cells. It requires interactions between adhesion receptors on endothelial cells and their counter-receptors on cancer cells. Notably, E-selectin, a major endothelial adhesion receptor, interacts with Death receptor-3 present on metastatic colon carcinoma cells. This interaction confers metastatic properties to colon cancer cells by promoting the adhesion of cancer cells to endothelial cells and triggering the activation of the pro-migratory p38 and pro-survival ERK pathways in the cancer cells. In the present study, we investigated further the mechanisms by which the E-selectin-activated pathways downstream of DR3 confer a survival advantage to colon cancer cells.
methodsCell survival has been ascertained by using the WST-1 assay and by evaluating the activation of the PI3 kinase/NFκB survival axis. Apoptosis has been assayed by determining DNA fragmentation by Hoechst staining and by measuring cleavage of caspases-8 and -3. DR3 isoforms have been identified by PCR. For more precise quantification, targeted PCR reactions were carried out, and the amplified products were analyzed by automated chip-based microcapillary electrophoresis on an Agilent 2100 Bioanalyzer instrument.
resultsInteraction between DR3-expressing HT29 colon carcinoma cells and E-selectin induces the activation of the PI3K/Akt pathway. Moreover, p65/RelA, the anti-apoptotic subunit of NFκB, is rapidly translocated to the nucleus in response to E-selectin. This translocation is impaired by the PI3K inhibitor LY294002. Furthermore, inhibition of the PI3K/Akt pathway increases the cleavage of caspase 8 in colon cancer cells treated with E-selectin and this effect is still further increased when both ERK and PI3K pathways are concomitantly inhibited. Intriguingly, metastatic colon cancer cell lines such as HT29 and SW620 express higher levels of a splice variant of DR3 that has no trans-membrane domain and no death domain.
conclusionColon cancer cells acquire an increased capacity to survive via the activation of the PI3K/NFκB pathway following the stimulation of DR3 by E-selectin. Generation of a DR3 splice variant devoid of death domain can further contribute to protect against apoptosis.
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