ArticleCell communication and signaling : CCS2017
DR5 suppression induces sphingosine-1-phosphate-dependent TRAF2 polyubiquitination, leading to activation of JNK/AP-1 and promotion of cancer cell invasion.
Article in Cell communication and signaling : CCS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- The role of ubiquitination in health and disease.MedComm · 2024Review
- System-wide identification of novel de-ubiquitination targets for USP10 in gastric cancer metastasis through multi-omics screening.BMC cancer · 2024Article
- Review
- Regulation of Cancer Metastasis by TRAIL/Death Receptor Signaling.Biomolecules · 2021Review
- Role of inflammatory microenvironment: potential implications for improved breast cancer nano-targeted therapy.Cellular and molecular life sciences : CMLS · 2021Review
- NVP-BEZ235 Inhibits Renal Cell Carcinoma by Targeting TAK1 and PI3K/Akt/mTOR Pathways.Frontiers in pharmacology · 2021Article
- Herpud1 deficiency could reduce amyloid-β40 expression and thereby suppress homocysteine-induced atherosclerosis by blocking the JNK/AP1 pathway.Journal of physiology and biochemistry · 2020Article
- Lysophospholipids and Their G-Coupled Protein Signaling in Alzheimer's Disease: From Physiological Performance to Pathological Impairment.Frontiers in molecular neuroscience · 2020Article
- The Tumorigenic Effect of Sphingosine Kinase 1 and Its Potential Therapeutic Target.Cancer control : journal of the Moffitt Cancer CenterReview
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDeath receptor (DR5), a well-characterized death domain-containing cell surface pro-apoptotic protein, has been suggested to suppress cancer cell invasion and metastasis. However, the underlying mechanisms have not been fully elucidated. Our recent work demonstrates that DR5 suppression promotes cancer cell invasion and metastasis through caspase-8/TRAF2-mediated activation of ERK and JNK signaling and MMP1 elevation. The current study aimed at addressing the mechanism through which TRAF2 is activated in a caspase-8 dependent manner.
resultsDR5 knockdown increased TRAF2 polyubiquitination, a critical event for TRAF2-mediated JNK/AP-1 activation. Suppression of sphingosine-1-phosphate (S1P) generation or depletion of casapse-8 inhibited not only enhancement of cell invasion, but also elevation and polyubiquitination of TRAF2, activation of JNK/AP-1 activation and increased expression of MMP1 induced by DR5 knockdown.
conclusionsBoth S1P and caspase-8 are critical for TRAF2 stabilization, polyubiquitination, subsequent activation of JNK/AP1 signaling and MMP1 expression and final promotion of cell invasion.
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