ArticleCancer science2022
Dvl2 facilitates the coordination of NF-κB and Wnt signaling to promote colitis-associated colorectal progression.
Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- The Barrier-Microbiota-Inflammation Axis in Colorectal Cancer: Mechanisms and Emerging Diagnostic & Therapeutic Strategies.Cancers · 2026Review
- Exploring the frontier of oral nanomedicine in colorectal cancer therapy: Folate-targeted 5FU-Nisin-Selenium conjugates and probiotic-rich diets as a novel approach.Asian journal of pharmaceutical sciences · 2025Article
- GIV/Girdin Modulation of Microglial Activation in Ischemic Stroke: Impact of FTO-Mediated m6A Modification.Molecular neurobiology · 2025Article
- CD44British journal of cancer · 2025Article
- Ivermectin inhibits epithelial-to-mesenchymal transition via Wnt signaling in endocrine-resistant breast cancer cells.PloS one · 2025Article
- Review
- Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024Review
- Review
- Protective Effect of Qingchang Wenzhong Decoction on Colitis and Colitis-Related Carcinogenesis by Regulating Inflammation and Intestinal Fibrosis.Journal of inflammation research · 2023Article
- Oncogenic and Receptor-Mediated Wnt Signaling Influence the Sensitivity of Colonic Cells to Butyrate.Journal of Cancer · 2023Article
- FOXK2 transcription factor and its roles in tumorigenesis (Review).Oncology letters · 2022Review
- Dvl2 facilitates the coordination of NF-κB and Wnt signaling to promote colitis-associated colorectal progression.Cancer science · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Colitis-associated colorectal cancer (CAC) arises due to prolonged inflammation and has distinct molecular events compared with sporadic colorectal cancer (CRC). Although inflammatory NF-κB signaling was activated by pro-inflammatory cytokines (such as TNFα) in early stages of CAC, Wnt/β-catenin signaling later appears to function as a key regulator of CAC progression. However, the exact mechanism responsible for the cross-regulation between these 2 pathways remains unclear. Here, we found reciprocal inhibition between NF-κB and Wnt/β-catenin signaling in CAC samples, and the Dvl2, an adaptor protein of Wnt/β-catenin signaling, is responsible for NF-κB inhibition. Mechanistically, Dvl2 interacts with the C-terminus of tumor necrosis factor receptor 1 (TNFRI) and mediates TNFRI endocytosis, leading to NF-κB signal inhibition. In addition, increased infiltration of the pro-inflammatory cytokine interleukin-13 (IL-13) is responsible for upregulating Dvl2 expression through STAT6. Targeting STAT6 effectively decreases Dvl2 levels and restrains colony formation of cancer cells. These findings demonstrate a unique role for Dvl2 in TNFRI endocytosis, which facilitates the coordination of NF-κB and Wnt to promote CAC progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.