ArticleOncology letters2022
Analysis of the expression, function and signaling of glycogen phosphorylase isoforms in hepatocellular carcinoma.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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.
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
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.
- Brain-Type Glycogen Phosphorylase (PYGB) in the Pathologies of Diseases: A Systematic Review.Cells · 2024Pooled it
- Mitochondria related gene signature serves as prognosis prediction and risk stratification of cholangiocarcinoma.Translational cancer research · 2026Article
- Metabolic buffering restricts phenotype switching in melanoma.The EMBO journal · 2026Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycogen phosphorylase (GP) is an essential enzyme for glycolysis via the glycogen degradation pathway. It consists of three isoforms: PYGB (brain form), PYGL (liver form) and PYGM (muscle form). Although the abnormal expression of GP is associated with a variety of tumors, its relationship with hepatocellular carcinoma (HCC) and whether it can be used as a prognostic marker of HCC remains unclear. In the present study, the expression levels of PYGB, PYGL and PYGM were analyzed. It was found that the expression levels of PYGB in tumor tissues were higher than those in normal tissues, particularly in HCC. The high expression of PYGB (hazard ratios=1.801; 95% confidence interval: 1.266-2.562) could predict the poor prognosis of HCC patients but not PYGL and PYGM. Inhibition of PYGB with GP inhibitor CP91149 significantly suppressed the HCC cell proliferation in the HCC cell model. In addition, combination treatment with sorafenib, a standard treatment for HCC, showed a great inhibition on tumor growth and angiogenesis. These findings suggested that PYGB may be used as a therapeutic and prognostic indicator for HCC.
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Registered trials
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