Lack of gp130 expression in hepatocytes attenuates tumor progression in the DEN model
Open accessAbstract
Chronic liver inflammation is a crucial event in the development and growth of hepatocellular carcinoma (HCC). Compelling evidence has shown that interleukin-6 (IL-6)/gp130-dependent signaling has a fundamental role in liver carcinogenesis. Thus, in the present study we aimed to investigate the role of gp130 in hepatocytes for the initiation and progression of HCC. Hepatocyte-specific gp130 knockout mice (gp130 Δhepa) and control animals (gp130 f/f) were treated with diethylnitrosamine (DEN). The role of gp130 for acute injury (0–144 h post treatment), tumor initiation (24 weeks) and progression (40 weeks) was analyzed. After acute DEN-induced liver injury we observed a reduction in the inflammatory response in gp130 Δhepa animals as reflected by decreased levels of IL-6 and oncostatin M. The loss of gp130 slightly attenuated the initiation of HCC 24 weeks after DEN treatment. In contrast, 40 weeks after DEN treatment, male and female gp130 Δhepa mice showed smaller tumors and reduced tumor burden, indicating a role for hepatocyte-specific gp130 expression during HCC progression. Oxidative stress and DNA damage were substantially and similarly increased by DEN in both gp130 f/f and gp130 Δhepa animals. However, gp130 Δhepa livers revealed aberrant STAT5 activation and decreased levels of transforming growth factor-β (TGF β), pSMAD2/3 and SMAD2, whereas phosphorylation of STAT3 at Tyr705 and Ser727 was absent. Our results indicate that gp130 deletion in hepatocytes reduces progression, but not HCC initiation in the DEN model. Gp130 deletion resulted in STAT3 inhibition but increased STAT5 activation and diminished TGF-dependent signaling. Hence, blocking gp130 in hepatocytes might be an interesting therapeutic target to inhibit the growth of HCC.
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IL-6 or gp130 knockout mice develop significantly fewer tumors in DEN-induced HCC model and have prolonged survival.
“Indeed, IL-6 or gp130 knockout mice developed significantly less tumors in the diethylnitrosamine (DEN)-induced HCC model and prolonged survival [63, 64]”
From The double-edged effects of IL-6 in liver regeneration, aging, inflammation, and diseases (2024) · cites this paper as [64]
The Results section ('Ablation of gp130 in hepatocytes reduces HCC progression in male and female mice'; page unavailable) reports significantly fewer tumor nodules in male mice with hepatocyte-specific gp130 deletion 40 weeks after DEN treatment. The reduction in female mice was not statistically significant. The paper does not report prolonged survival, and its own experiment did not test IL-6 knockout mice. (LLM, conf=0.88)
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Wang, F., Lim, E. B., Mehta, R., & Wu, Y. L. (2026) · Cell Biology International · doi:10.1002/cbin.70227
- Authors
- Hatting, M., Spannbauer, M., Peng, J., Al Masaoudi, M., Sellge, G., Nevzorova, Y. A., Gassler, N., Liedtke, C., Cubero, F. J., & Trautwein, C.
- Affiliations
- Universitätsklinikum Aachen (DE)
- Corresponding author
- Cubero, F J
- Trautwein, C
- Venue
- Cell Death & Disease
- Published
- 2015-03-05
- Volume
- 6
- Issue
- 3
- Pages
- e1667-e1667
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC4385909
- OpenAlex
- W1989521990
- Cited by
- 30
- References
- 59
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 1 · 2022: 5 · 2021: 5 · 2020: 1 · 2019: 4 · 2018: 4 · 2017: 1 · 2016: 6
- FWCI
- 1.60
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Death and Disease (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RWTH Publications (RWTH Aachen) (submittedVersion, other-oa)
- RWTH Publications (RWTH Aachen)
- Funders
- Deutsche Forschungsgemeinschaft (107682)
- Deutsche Krebshilfe (107682)
- RWTH Aachen University
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
- Keywords
- gp130, hepatocellular carcinoma, hepatocytes, diethylnitrosamine, hepatocarcinogenesis, IL-6 signaling, STAT5, STAT3, TGF-beta signaling, oncostatin M, chronic liver inflammation, hepatocyte-specific knockout mice, tumor progression, oxidative stress, DNA damage
- MeSH terms
- Animals, Diethylnitrosamine, DNA Damage, Female, Flow Cytometry, Fluorescent Antibody Technique, Carcinoma, Hepatocellular, Inflammation, Male, Mice, Inbred C57BL, Immunoblotting, Mice, Knockout, Oxidative Stress, Hepatocytes, STAT3 Transcription Factor, STAT5 Transcription Factor, Cytokine Receptor gp130, Mice, Oncostatin M
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