ArticleCarcinogenesis2015
Tumor-promoting/progressing role of additional chromosome instability in hepatic carcinogenesis in Sgo1 (Shugoshin 1) haploinsufficient mice.
Article in Carcinogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed.
- Shugoshin 1 expression in various cancers: a potential target for therapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Arsenic and UVR co-exposure results in unique gene expression profile identifying key co-carcinogenic mechanisms.Toxicology and applied pharmacology · 2024Article
- Genomic instability genes in lung and colon adenocarcinoma indicate organ specificity of transcriptomic impact on Copy Number Alterations.Scientific reports · 2022Article
- Identification and validation of a potential key gene SGOL1 for poor prognosis in hepatocellular carcinoma based on a bioinformatics approach.Frontiers in oncology · 2022Article
- Article
- Survival-Critical Genes Associated with Copy Number Alterations in Lung Adenocarcinoma.Cancers · 2021Article
- GSK3-ARC/Arg3.1 and GSK3-Wnt signaling axes trigger amyloid-β accumulation and neuroinflammation in middle-aged Shugoshin 1 mice.Aging cell · 2020Article
- Role of E2Fs and mitotic regulators controlled by E2Fs in the epithelial to mesenchymal transition.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- The expanding phenotypes of cohesinopathies: one ring to rule them all!Cell cycle (Georgetown, Tex.) · 2019Review
- SGO1 induces proliferation and metastasis of prostate cancer through AKT-mediated signaling pathway.American journal of cancer research · 2019Article
- Overexpression of shugoshin1 predicts a poor prognosis for prostate cancer and promotes metastasis by affecting epithelial-mesenchymal transition.OncoTargets and therapy · 2019Article
- Spontaneous development of Alzheimer's disease-associated brain pathology in a Shugoshin-1 mouse cohesinopathy model.Aging cell · 2018Article
- Critical role of mitosis in spontaneous late-onset Alzheimer's disease; from a Shugoshin 1 cohesinopathy mouse model.Cell cycle (Georgetown, Tex.) · 2018Review
- A novel microRNAs expression signature for hepatocellular carcinoma diagnosis and prognosis.Oncotarget · 2017Article
- Frequently mutated genes/pathways and genomic instability as prevention targets in liver cancer.Carcinogenesis · 2017Review
- Article
- Systemic Chromosome Instability Resulted in Colonic Transcriptomic Changes in Metabolic, Proliferation, and Stem Cell Regulators in Sgo1-/+ Mice.Cancer research · 2016Article
- Hepatocellular carcinoma mouse models: Hepatitis B virus-associated hepatocarcinogenesis and haploinsufficient tumor suppressor genes.World journal of gastroenterology · 2016Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
A major etiological risk factor for hepatocellular carcinoma (HCC) is infection by Hepatitis viruses, especially hepatitis B virus and hepatitis C virus. Hepatitis B virus and hepatitis C virus do not cause aggressive activation of an oncogenic pathway, but they transactivate a broad array of genes, cause chronic inflammation, and, through interference with mitotic processes, lead to mitotic error-induced chromosome instability (ME-CIN). However, how ME-CIN is involved in the development of HCC remains unclear. Delineating the effect of ME-CIN on HCC development should help in identifying measures to combat HCC. In this study, we used ME-CIN model mice haploinsufficient in Shugoshin 1 (Sgo1(-/+)) to assess the role of ME-CIN in HCC development. Treatment with the carcinogen azoxymethane caused Sgo1(-/+) ME-CIN model mice to develop HCCs within 6 months, whereas control mice developed no HCC (P < 0.003). The HCC development was associated with expression of early HCC markers (glutamine synthetase, glypican 3, heat shock protein 70, and the serum marker alpha fetoprotein), although without fibrosis. ME-CIN preceded the expression of HCC markers, suggesting that ME-CIN is an important early event in HCC development. In 12-month-old untreated Sgo1 mice, persistent DNA damage, altered gene expression, and spontaneous HCCs were observed. Sgo1 protein accumulated in response to DNA damage in vitro. Overall, Sgo1(-/+)-mediated ME-CIN strongly promoted/progressed development of HCC in the presence of an initiator carcinogen, and it had a mild initiator effect by itself. Use of the ME-CIN model mice should help in identifying drugs to counteract the effects of ME-CIN and should accelerate anti-HCC drug development.
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