ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Tribbles Pseudokinase 3 Converts Sorafenib Therapy to Neutrophil-Mediated Lung Metastasis in Hepatocellular Carcinoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Glutamine Deprivation Triggers Tribbles Homolog 3 Dependent G-Quadruplex Resolution to Maintain DNA Repair and Tumor Survival.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Therapy-induced remodeling of the tumor immune microenvironment: Mechanistic insights and implications for immunotherapy.Chinese medical journal · 2026Review
- TONSL promotes hepatocellular carcinoma progression and radioresistance by orchestrating DNA damage repair and cell cycle dynamics.Discover oncology · 2026Article
- Psammaplysene D overcomes sorafenib resistance in liver cancer by targeting FGFR4/CYP26A1-retinoic acid axis to drive ferroptosis.Journal of experimental & clinical cancer research : CR · 2026Article
- Combination therapy with Nifuroxazide and Lenvatinib exerts superior anti-hepatocellular carcinoma effect by enhancing the anti-tumor immune response.Frontiers in oncology · 2026Article
- Bioengineered Exosome-Magnetic Nanoplatform for Precision Therapy of Hepatocellular CarcinomaInternational journal of nanomedicine · 2026Article
- Neutrophil Extracellular Trap Reprograms Cancer Metabolism to Form a Metastatic Niche Promoting Non-Small Cell Lung Cancer Brain Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Kuwanon A Targeted YWHAB in Hepatocellular Carcinoma Cells to Inhibit the Raf/MEK/ERK Signaling Pathway.Cells · 2025Article
- Targeting mitochondrial dysfunction to intervene in liver cancer.Cancer biology & medicine · 2025Review
- CD24 recruits tumor-associated neutrophils to promote the progression of hepatocellular carcinoma.Journal for immunotherapy of cancer · 2025Article
- MET promotes hepatocellular carcinoma development through the promotion of TRIB3-mediated FOXO1 degradation.Clinical and molecular hepatology · 2025Article
- Tribbles Pseudokinase 3 Converts Sorafenib Therapy to Neutrophil-Mediated Lung Metastasis in Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Single-cell transcriptomics identifies anFrontiers in molecular biosciences · 2025Article
- Indoleamine 2,3-dioxygenase-galectin-3 fusion protein remodels inflammatory and fibrotic programs, ameliorating imiquimod-induced psoriasis.npj biomedical innovations · 2025Article
- Unraveling the alterations and biomarkers in the tumor microenvironment in lung adenocarcinoma metastases and their indications for therapeutic response and prognosis.Therapeutic advances in medical oncology · 2025Review
- Novel Strategies against Hepatocellular Carcinoma through Lipid Metabolism.Oncology research · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Rapid development of resistance to sorafenib and subsequent hyperprogression in patients with advanced hepatocellular carcinoma (HCC) pose significant challenges, with the underlying mechanisms still largely unknown. Herein, sorafenib-induced TRIB3 is identified as a liver-specific determinant driving secondary resistance to sorafenib by facilitating the accumulation of protumorigenic neutrophils within tumors. Mechanistically, TRIB3, triggered by the sorafenib-elicited ROS-ER stress axis, operates in an NF-κB-dependent manner to upregulate CXCR1/2 ligands, subsequently promoting neutrophil recruitment into tumors. These enriched neutrophils enhance epithelial-mesenchymal transition processes in malignant cells through the oncostatin M-STAT3 pathway, thereby repurposing the therapeutic efficacy of sorafenib away from anti-angiogenesis and toward lung metastasis. Clinically, elevated TRIB3 expression indicates inferior survival and unfavorable clinical efficacy of sorafenib in HCC patients. Correspondingly, strategies that either inhibiting TRIB3 upregulation or blocking its downstream signaling successfully augment the therapeutic efficacy of sorafenib and prevent sorafenib-induced hyperprogression in vivo. The study thus identifies a pivotal mechanism of sorafenib resistance in HCC, centered on the TRIB3-mediated recruitment of protumorigenic neutrophils and subsequent disease hyperprogression.
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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.