ArticleCellular and molecular gastroenterology and hepatology2022
Antagonizing STK25 Signaling Suppresses the Development of Hepatocellular Carcinoma Through Targeting Metabolic, Inflammatory, and Pro-Oncogenic Pathways.
Article in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Targeting STE20-type kinase MST3 improves metabolic dysfunction-associated steatohepatitis without affecting hepatocellular carcinoma development in mice.BMC medicine · 2026Article
- STK25 Loss Augments Anti-PD-1 Therapy Efficacy by Regulating PD-L1 Stability in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Inhibition of GCKIII kinases STK25 and MST3 mitigates organ lipotoxicity and enhances metabolic resilience under nutritional stress.BMC medicine · 2025Article
- TLR-induced STK25 activation promotes IRF5-mediated inflammation.Life science alliance · 2025Article
- Advances in experimental animal models of hepatocellular carcinoma.Cancer medicine · 2023Review
- Emerging novel targets for nonalcoholic fatty liver disease treatment: Evidence from recent basic studies.World journal of gastroenterology · 2023Review
- Bioactive xanthones, benzophenones and biphenyls from mangosteen root with potential anti-migration against hepatocellular carcinoma cells.Scientific reports · 2022Article
- STK25 enhances hepatocellular carcinoma progression through the STRN/AMPK/ACC1 pathway.Cancer cell international · 2022Article
- Ste20-like Kinase STK25: A Potential Target in Prevention and Therapy of NASH-Associated Hepatocellular Carcinoma?Cellular and molecular gastroenterology and hepatology · 2022Article
- Disruption of Growth Hormone Receptor Signaling Abrogates Hepatocellular Carcinoma Development.Journal of hepatocellular carcinoma · 2022Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsHepatocellular carcinoma (HCC) is one of the most fatal and fastest-growing cancers. Recently, nonalcoholic steatohepatitis (NASH) has been recognized as a major catalyst for HCC. Thus, additional research is critically needed to identify mechanisms involved in NASH-induced hepatocarcinogenesis, to advance the prevention and treatment of NASH-driven HCC. Because the sterile 20-type kinase serine/threonine kinase 25 (STK25) exacerbates NASH-related phenotypes, we investigated its role in HCC development and aggravation in this study.
methodsHepatocarcinogenesis was induced in the context of NASH in Stk25 knockout and wild-type mice by combining chemical procarcinogens and a dietary challenge. In the first cohort, a single injection of diethylnitrosamine was combined with a high-fat diet-feeding. In the second cohort, chronic administration of carbon tetrachloride was combined with a choline-deficient L-amino-acid-defined diet. To study the cell-autonomous mode of action of STK25, we silenced this target in the human hepatocarcinoma cell line HepG2 by small interfering RNA.
resultsIn both mouse models of NASH-driven HCC, the livers from Stk25
conclusionsThis study provides evidence that antagonizing STK25 signaling hinders the development of NASH-related HCC and provides an impetus for further analysis of STK25 as a therapeutic target for NASH-induced HCC treatment in human beings.
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