ArticleJournal of experimental & clinical cancer research : CR2023
Paracrine activin B-NF-κB signaling shapes an inflammatory tumor microenvironment in gastric cancer via fibroblast reprogramming.
Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
- INHBB Promotes Colorectal Cancer Progression by Inducing CD8Cancer science · 2026Article
- Enhanced ITGA3 expression induced by helicobacter pylori infection facilitates gastric cancer progression via NF-κB and Smad4.Molecular and cellular biochemistry · 2026Article
- SLC41A2 Suppresses Colon Cancer Progression by Inhibiting GSK3β Ubiquitin-proteasome Degradation.Current molecular medicine · 2026Article
- Pathogenic role and therapeutic targets of nuclear factor-κB signaling pathway in cancer (Review).Oncology letters · 2025Review
- Targeting the NF-κB Pathway in Cancer: Mechanisms, Resistance, and Therapeutic Potential Across Tumor Types.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Activin B Regulates Fibroblasts to Promote Granulation Tissue Formation and Angiogenesis During Murine Skin-Wound Healing via the JNK/ERK Signaling Pathway.International journal of molecular sciences · 2025Article
- NKAPL suppresses NSCLC progression by enhancing the protein stability of TRIM21 and further inhibiting the NF-κB signaling pathway.Genes & diseases · 2025Article
- Decoding the Plasticity of Cancer-Associated Fibroblasts: Mechanistic Insights and Precision Targeting Strategies in Gastric Cancer Progression and Therapeutic Resistance.Cell proliferation · 2025Article
- Remdesivir inhibits endothelial activation and atherosclerosis by coupling TAL1 to TRAF6.Journal of translational medicine · 2025Article
- Neutrophil extracellular traps-related genes contribute to sepsis-associated acute kidney injury.BMC nephrology · 2025Article
- Mapping the landscape of gastric cancer immunotherapy: Bibliometric insights into advances and hotspots.World journal of gastrointestinal oncology · 2025Article
- Extracellular vesicles: messengers of cross-talk between gastric cancer cells and the tumor microenvironment.Frontiers in cell and developmental biology · 2025Review
- Multi-Omics Analysis Reveals the transforming growth factor-β Signaling-Driven Multicellular Interactions with Prognostic Relevance in Cervical Cancer Progression.Journal of Cancer · 2025Article
- Molecular Mechanism for Malignant Progression of Gastric Cancer Within the Tumor Microenvironment.International journal of molecular sciences · 2024Review
- Induced dual-target rebalance simultaneously enhances efficient therapeutical efficacy in tumors.Cell death discovery · 2024Article
- Combining single-cell analysis and molecular docking techniques to construct a prognostic model for colon adenocarcinoma and uncovering inhibin subunit βb as a novel therapeutic target.Frontiers in immunology · 2024Article
- Reprogramming of tumor-associated macrophages by metabolites generated from tumor microenvironment.Animal cells and systems · 2024Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundImportant roles of INHBB in various malignancies are increasingly identified. The underlying mechanisms in gastric cancer (GC) microenvironment are still greatly unexplored.
methodsThe clinical significance of INHBB and the correlation between INHBB and p-p65 in GC were assessed through analyzing publicly available databases and human paraffin embedded GC tissues. The biological crosstalk of INHBB between GC cells and fibroblasts was explored both in vitro and in vivo. RNA-seq analyses were performed to determine the mechanisms which regulating fibroblasts reprogramming. Luciferase reporter assay and chromatin immunoprecipitation (CHIP) assay were used to verify the binding relationship of p65 and INHBB in GC cells.
resultsOur study showed that INHBB level was significantly higher in GC, and that increased INHBB was associated with poor survival. INHBB positively regulates the proliferation, migration, and invasion of GC cells in vitro. Also, activin B promotes the occurrence of GC by reprogramming fibroblasts into cancer-associated fibroblasts (CAFs). The high expression of INHBB in GC cells activates the NF-κB pathway of normal gastric fibroblasts by secreting activin B, and promotes fibroblasts proliferation, migration, and invasion. In addition, activin B activates NF-κB pathway by controlling TRAF6 autoubiquitination to induce TAK1 phosphorylation in fibroblasts. Fibroblasts activated by activin B can induce the activation of p65 phosphorylation of GC cells by releasing pro-inflammatory factors IL-1β. p65 can directly bind to the INHBB promoter and increase the INHBB transcription of GC cells, thus establishing a positive regulatory feedback loop to promote the progression of GC.
conclusionsGC cells p65/INHBB/activin B and fibroblasts p65/IL-1β signal loop led to the formation of a whole tumor-promoting inflammatory microenvironment, which might be a promising therapeutic target for GC.
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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 Socratic graph.