ArticleJournal of cell communication and signaling2019
TGF-β1 and TNF-α synergistically induce epithelial to mesenchymal transition of breast cancer cells by enhancing TAK1 activation.
Article in Journal of cell communication and signaling, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Transforming growth factor-β and integrins: key players in EMT and breast cancer progression.Cancer cell international · 2026Review
- Single amino-acid differences define H2B variants and modify chromatin accessibility to induce EMT in breast cancer.Oncogene · 2026Article
- Single-cell multiomic modelling of early metastatic events promoted by the extracellular matrix.British journal of cancer · 2025Article
- Stem cell- and extracellular vesicle-based therapies for perianal fistulizing Crohn's disease: An updated review.World journal of gastroenterology · 2025Review
- TGFβ1-TNFα-regulated secretion of neutrophil chemokines is independent of epithelial-mesenchymal transition in breast tumor cells.Molecular biology of the cell · 2025Article
- Dynamics of epithelial-mesenchymal plasticity driving cancer drug resistance.Cancer pathogenesis and therapy · 2025Review
- Phenomics Demonstrates Cytokines Additive Induction of Epithelial to Mesenchymal Transition.Journal of cellular physiology · 2025Article
- Comprehensive molecular interaction map of TGFβ induced epithelial to mesenchymal transition in breast cancer.NPJ systems biology and applications · 2024Article
- Lactate dehydrogenase A promotes nasopharyngeal carcinoma progression through the TAK1/NF-κB Axis.Molecular biology reports · 2024Article
- TGF-β and TNF-α interaction promotes the expression of MMP-9 through H3K36 dimethylation: implications in breast cancer metastasis.Frontiers in immunology · 2024Article
- Potential role of epithelial-mesenchymal transition induced by periodontal pathogens in oral cancer.Journal of cellular and molecular medicine · 2024Review
- Article
- Molecular Evaluation of the Impact of Polymorphic Variants in Apoptotic (Current issues in molecular biology · 2023Article
- β-Catenin signaling in alveolar macrophages enhances lung metastasis through a TNF-dependent mechanism.JCI insight · 2023Article
- Chondroitin polymerizing factor predicts a poor prognosis and promotes breast cancer progression via the upstream TGF-β1/SMAD3 and JNK axis activation.Journal of cell communication and signaling · 2023Article
- Medicine Targeting Epithelial-Mesenchymal Transition to Treat Airway Remodeling and Pulmonary Fibrosis Progression.Canadian respiratory journal · 2023Review
- Zengshengping improves lung cancer by regulating the intestinal barrier and intestinal microbiota.Frontiers in pharmacology · 2023Article
- Tumor necrosis factor-α coordinates with transforming growth factor-β1 to induce epithelial-mesenchymal transition and migration via the NF-κB/NOX4 pathway in bronchial epithelial cells.Molecular biology reports · 2022Article
- Paclitaxel resistance is mediated by NF-κB on mesenchymal primary breast cancer cells.Oncology letters · 2022Article
- Relationship between serum TGF- β 1, MMP-9 and IL-1β and pathological features and prognosis in breast cancer.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
TGF-β1 is a main inducer of epithelial to mesenchymal transition (EMT). However, many breast cancer cells are not sensitive to the EMT induction by TGF-β1 alone. So far, the mechanisms underlying the induction of TGF-β1-insensitive breast cancer cells remains unclear. Here we report that TNF-α can induce EMT and invasiveness of breast cancer cells which are insensitive to TGF-β1. Intriguingly, TGF-β1 could cooperate with TNF-α to promote the EMT and invasiveness of breast cancer cells. The prolonged co-stimulation with TGF-β1 and TNF-α could enhance the sustained activation of Smad2/3, p38 MAPK, ERK, JNK and NF-κB pathways by enhancing the activation of TAK1, which was mediated by the gradually up-regulated TβRs. Except for JNK, all of these pathways were required for the effects of TGF-β1 and TNF-α. Importantly, the activation of p38 MAPK and ERK pathways resulted in a positive feed-back effect on TAK1 activation by up-regulating the expression of TβRs, favoring the activation of multiple signaling pathways. Moreover, SLUG was up-regulated and required for the TGF-β1/TNF-α-induced EMT and invasiveness. In addition, SLUG could also enhance the activation of signaling pathways by promoting TβRII expression. These findings suggest that the up-regulation of TβRs contributes to the sustained activation of TAK1 induced by TGF-β1/TNF-α and the following activation of multiple signaling pathways, resulting in EMT and invasiveness of breast cancer cells.
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