ArticleInternational journal of molecular sciences2024
Role of Epiregulin on Lipopolysaccharide-Induced Hepatocarcinogenesis as a Mediator via EGFR Signaling in the Cancer Microenvironment.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 4 citations in OpenAlex.
- A bioengineered platform reveals progressive impairment of skeletal muscles by metabolic dysfunction-associated steatotic liver disease-derived factors.Disease models & mechanisms · 2026Article
- Polysaccharides: Natural candidates for targeting immunometabolic regulation in hepatocellular carcinoma (Review).Molecular medicine reports · 2026Review
- Developing a Clinically Practical Biomaterial Platform for Endogenous Liver Regeneration.Gels (Basel, Switzerland) · 2026Review
- Review
- The landscape of gut microbiota in hepatocarcinogenesis: a comprehensive review of pathogenesis and therapeutic interventions.International journal of surgery (London, England) · 2026Review
- New insights into the effects of microbiome and its derived metabolites on targeted immunotherapy.Journal of the Egyptian National Cancer Institute · 2025Review
- Rifaximin Attenuates Liver Fibrosis and Hepatocarcinogenesis in a Rat MASH Model by Suppressing the Gut-Liver Axis and Epiregulin-IL-8-Associated Angiogenesis.International journal of molecular sciences · 2025Article
- The interplay between gut bacteria and targeted therapies: implications for future cancer treatments.Molecular medicine (Cambridge, Mass.) · 2025Review
- Insights into the gut-liver axis: mechanisms and emerging therapies in hepatocellular carcinoma.Frontiers in pharmacology · 2025Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Lipopolysaccharides (LPSs) have been reported to be important factors in promoting the progression of hepatocellular carcinoma (HCC), but the corresponding molecular mechanisms remain to be elucidated. We hypothesize that epiregulin (EREG), an epidermal growth factor (EGF) family member derived from hepatic stellate cells (HSCs) and activated by LPS stimulation, is a crucial mediator of HCC progression with epidermal growth factor receptor (EGFR) expression in the tumor microenvironment. We used a mouse xenograft model of Huh7 cells mixed with half the number of LX-2 cells, with/without intraperitoneal LPS injection, to elucidate the role of EREG in LPS-induced HCC. In the mouse model, LPS administration significantly enlarged the size of xenografted tumors and elevated the expression of EREG in tumor tissues compared with those in negative controls. Moreover, CD34 immunostaining and the gene expressions of angiogenic markers by a reverse transcription polymerase chain reaction revealed higher vascularization, with increased interleukin-8 (IL-8) expression in the tumors of the mice group treated with LPS compared to those without LPS. Our data collectively suggested that EREG plays an important role in the cancer microenvironment under the influence of LPS to increase not only the tumor cell growth and migration/invasion of EGFR-positive HCC cells but also tumor neovascularization via IL-8 signaling.
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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.