ArticleNature communications2017
Autophagy acts through TRAF3 and RELB to regulate gene expression via antagonism of SMAD proteins.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Autophagy maintains high endothelial venule identity and function during inflammation.Immunity · 2026Article
- A single mutation in nonstructural protein 1 is critical for the adaptive evolution of influenza B virus.Nature communications · 2026Article
- USP15-dependent modulation of TGF-β/Smad2/3 signaling: implications for chondrocyte matrix degradation and autophagy in osteoarthritis.Scientific reports · 2025Article
- Cell Settling, Migration, and Stochastic Cancer Gene Expression Suggest Potassium Membrane Flux May Initiate pH Reversal.Biomolecules · 2025Article
- [Comprehensive Analysis of the Expression, Prognosis and Function of TRAF Family Proteins in NSCLC].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Article
- Autophagy in the lung: guardian of homeostasis or driver of disease.Autophagy reports · 2025Review
- Selective degradation of PL2L60 by metabolic stresses‑induced autophagy suppresses multi‑cancer growth.Oncology reports · 2024Article
- TRAF3/STAT6 axis regulates macrophage polarization and tumor progression.Cell death and differentiation · 2023Article
- Autophagy/Mitophagy Regulated by Ubiquitination: A Promising Pathway in Cancer Therapeutics.Cancers · 2023Review
- The Roles of TRAF3 in Immune Responses.Disease markers · 2023Review
- Modulating glycosphingolipid metabolism and autophagy improves outcomes in pre-clinical models of myeloma bone disease.Nature communications · 2022Article
- Role of AMPK in autophagy.Frontiers in physiology · 2022Review
- Kartogenin Improves Osteogenesis of Bone Marrow Mesenchymal Stem Cells via Autophagy.Stem cells international · 2022Article
- Crosstalk Between NDP52 and LUBAC in Innate Immune Responses, Cell Death, and Xenophagy.Frontiers in immunology · 2021Article
- Trehalose attenuates TGF-β1-induced fibrosis of hSCFs by activating autophagy.Molecular and cellular biochemistry · 2020Article
- SMAD4 activates Wnt signaling pathway to inhibit granulosa cell apoptosis.Cell death & disease · 2020Article
- Life, death, and autophagy in cancer: NF-κB turns up everywhere.Cell death & disease · 2020Review
- The MDM2 ligand Nutlin-3 differentially alters expression of the immune blockade receptors PD-L1 and CD276.Cellular & molecular biology letters · 2020Article
- Pro-Tumoral Functions of Autophagy Receptors in the Modulation of Cancer Progression.Frontiers in oncology · 2020Review
- Transcriptome analysis reveals autophagy as regulator of TGFβ/Smad-induced fibrogenesis in trabecular meshwork cells.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Macroautophagy can regulate cell signalling and tumorigenesis via elusive molecular mechanisms. We establish a RAS mutant cancer cell model where the autophagy gene ATG5 is dispensable in A549 cells in vitro, yet promotes tumorigenesis in mice. ATG5 represses transcriptional activation by the TGFβ-SMAD gene regulatory pathway. However, autophagy does not terminate cytosolic signal transduction by TGFβ. Instead, we use proteomics to identify selective degradation of the signalling scaffold TRAF3. TRAF3 autophagy is driven by RAS and results in activation of the NF-κB family member RELB. We show that RELB represses TGFβ target promoters independently of DNA binding at NF-κB recognition sequences, instead binding with SMAD family member(s) at SMAD-response elements. Thus, autophagy antagonises TGFβ gene expression. Finally, autophagy-deficient A549 cells regain tumorigenicity upon SMAD4 knockdown. Thus, at least in this setting, a physiologic function for autophagic regulation of gene expression is tumour growth.
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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.