ArticleAmerican journal of cancer research2025
Cytoglobin suppresses oxidative damage and compensatory proliferation via inhibiting AKT/ERK1/2/CyclinD1 axis in hepatocellular carcinoma.
Article in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Therapeutic Potential of Cytoglobin and Neuroglobin in Oxidative Stress-Driven Liver Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Cytoglobin in Hepatic Stellate Cells Plays Anti-Fibrotic Role in Chronic Liver Injury.Antioxidants (Basel, Switzerland) · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chronic liver injury caused by diverse etiologies provokes abnormal compensatory proliferation and contributes to hepatocarcinogenesis. Oxidative stress (OS) is an independent etiology which induces cell injury and triggers oncogenes activation and tumor suppressor genes dysfunction. Cytoglobin (CYGB) is a member of the human hexacoordinate hemoglobin (HHB) family and functions as a dynamic antioxidant enzyme. We previously reported that CYGB decreases the intracellular ROS/RNS level and inhibits HCC proliferation and stemness under normal oxidative level. In this study, we observed that CYGB is decreased in HCC tissues, particularly in tumors with p53 mutations. Its deficiency is associated with advanced stage, elevated Ki-67 proliferation index, and predicts a worse prognosis in HCC patients. Ectopic CYGB expression attenuates malondialdehyde (MDA) level and AST/ALT release, as well reduces apoptosis and subG1 percentage and simultaneously induces G1 arrest in pre-H
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