ArticlePloS one2015
Growth Arrest Specific 1 (Gas1) Gene Overexpression in Liver Reduces the In Vivo Progression of Murine Hepatocellular Carcinoma and Partially Restores Gene Expression Levels.
Article in PloS one, 2015. 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, 21 citations in OpenAlex.
- Gas1-Mediated Suppression of Hepatoblastoma Tumorigenesis.The American journal of pathology · 2025Article
- Transcriptomic landscape of Hras12V oncogene-induced hepatocarcinogenesis with gender disparity.BMC cancer · 2025Article
- GAS1 Promotes Ferroptosis of Liver Cells in Acetaminophen-Induced Acute Liver Failure.International journal of medical sciences · 2023Article
- EGR1 as a potential marker of prognosis in extranodal NK/T-cell lymphoma.Scientific reports · 2021Article
- Reporting animal research: Explanation and elaboration for the ARRIVE guidelines 2.0.PLoS biology · 2020Article
- ZNF518B gene up-regulation promotes dissemination of tumour cells and is governed by epigenetic mechanisms in colorectal cancer.Scientific reports · 2019Article
- Deoxynivalenol- and zearalenone-contaminated feeds alter gene expression profiles in the livers of piglets.Asian-Australasian journal of animal sciences · 2018Article
- Role of early growth response 1 in liver metabolism and liver cancer.Hepatoma research · 2017Article
- GAS1 is present in the cerebrospinal fluid and is expressed in the choroid plexus of the adult rat.Histochemistry and cell biology · 2016Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prognosis of hepatocellular carcinoma patients is usually poor, the size of tumors being a limiting factor for surgical treatments. Present results suggest that the overexpression of Gas1 (growth arrest specific 1) gene reduces the size, proliferating activity and malignancy of liver tumors. Mice developing diethylnitrosamine-induced hepatocellular carcinoma were subjected to hydrodynamic gene delivery to overexpress Gas1 in liver. This treatment significantly (p < 0.05) reduced the number of large tumors, while the difference in the total number of lesions was not significant. Moreover, the number of carcinoma foci in the liver and the number of lung metastases were reduced. These results are related with the finding that overexpression of Gas1 in Hepa 1-6 cells arrests cell cycle before S phase, with a significant (p < 0.01) and concomitant reduction in the expression of cyclin E2 gene. In addition, a triangular analysis of microarray data shows that Gas1 overexpression restores the transcription levels of 150 genes whose expression was affected in the diethylnitrosamine-induced tumors, thirteen of which are involved in the hedgehog signaling pathway. Since the in vivo Gas1 gene delivery to livers of mice carrying hepatocellular carcinoma reduces the size and proliferating activity of tumors, partially restoring the transcriptional profile of the liver, the present study opens promising insights towards a therapeutic approach for hepatocellular carcinoma.
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