ArticleCancer cell2014
ER stress cooperates with hypernutrition to trigger TNF-dependent spontaneous HCC development.
Article in Cancer cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 347 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
347 citing papers in PubMed, 2 syntheses or guidelines pooled it, 520 citations in OpenAlex.
- Evidence-based clinical practice guidelines for metabolic dysfunction-associated steatotic liver disease (MASLD) 2026.Journal of gastroenterology · 2026Guideline
- Obesity-related gut hormones and cancer: novel insight into the pathophysiology.International journal of obesity (2005) · 2021Pooled it
- Reduction of Hepatic Fat Content by Dulaglutide for the Treatment of Diabetes Mellitus: A Two-Centre Open, Single-Arm Trial.Endocrinology, diabetes & metabolism · 2025Trial
- Immune checkpoints and immunoregulation in metabolic diseases and cancers: pathological mechanisms and therapeutic potential.Signal transduction and targeted therapy · 2026Review
- Biogenesis of TNF-α-insights into proteostasis and inflammation.The FEBS journal · 2026Review
- Nano-formulations in therapeutic strategies targeting cancer ferroptosis.Journal of pharmaceutical analysis · 2026Review
- SREBP-driven lipogenesis coupled with ferroptosis resistance as a therapeutic target in PTEN-loss extrahepatic cholangiocarcinoma.JHEP reports : innovation in hepatology · 2026Article
- A multi-functional oral small molecule targeting energy and lipid metabolism to treat obesity and related metabolic disorders.Science advances · 2026Article
- Adaptive oncogenesis of β-catenin emerges from declining liver tissue integrity.Nature communications · 2026Article
- The Regeneration Paradox in Liver Cancer: How Chronic Injury Transforms Healing into Carcinogenesis.Liver cancer · 2026Review
- The versatile interplay between steatotic liver disease and liver cancer.Nature reviews. Cancer · 2026Review
- Ferroptosis-driven metabolic reprogramming in macrophages: Reshaping glucose utilization landscapes.Chinese medical journal · 2026Review
- Impaired glycosylation promotes rapid transition to hepatocellular carcinoma in model of diet-induced steatotic liver disease.The Journal of clinical investigation · 2026Article
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- Multi-omics profiling reveals divergent biology and liver microenvironment in HCC of metastatic and de novo origin.Molecular cancer · 2026Article
- Article
- Sexual Dimorphism in the Initial Apoptotic Switch During MASH Progression in Mice.International journal of molecular sciences · 2026Article
- The Role of Kupffer Cells and Liver Macrophages in the Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomedicines · 2026Review
- A Mouse in vivo Model Mimicking MASH-Related HCC Pathogenesis.Journal of hepatocellular carcinoma · 2026Article
- Etiology-Driven Mouse Models of Hepatocellular Carcinoma: Paving the Way for Precision Oncology.Journal of hepatocellular carcinoma · 2026Review
287 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
Endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of viral hepatitis, insulin resistance, hepatosteatosis, and nonalcoholic steatohepatitis (NASH), disorders that increase risk of hepatocellular carcinoma (HCC). To determine whether and how ER stress contributes to obesity-driven hepatic tumorigenesis we fed wild-type (WT) and MUP-uPA mice, in which hepatocyte ER stress is induced by plasminogen activator expression, with high-fat diet. Although both strains were equally insulin resistant, the MUP-uPA mice exhibited more liver damage, more immune infiltration, and increased lipogenesis and, as a result, displayed classical NASH signs and developed typical steatohepatitic HCC. Both NASH and HCC development were dependent on TNF produced by inflammatory macrophages that accumulate in the MUP-uPA liver in response to hepatocyte ER stress.
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What OpenQuestion holds
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.