ArticleJournal of gastrointestinal oncology2023
NDRG2 inhibition of glycolysis in liver tumor cells is regulated by SIRT1.
Article in Journal of gastrointestinal oncology, 2023. 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, 3 citations in OpenAlex.
- Cysteine protease inhibitor 1 promotes metastasis by mediating an oxidative phosphorylation/MEK/ERK axis in esophageal squamous carcinoma cancer.Scientific reports · 2024Article
- A New Frontier in Phytotherapy: Harnessing the Therapeutic Power of Medicinal Herb-derived miRNAs.Current pharmaceutical design · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: N-Myc downstream-regulated gene 2 (NDRG2) is a tumor suppressor, highly expressed in normal tissues but downregulated in many cancers. However, it has been shown to be involved in regulating glycolytic enzymes in clear cell renal cell carcinoma and colorectal cancer, although the mechanism is still not clear, and the function of NDRG2 in liver tumor glycolysis is completely unknown. Methods: Liver tumor tissues were obtained from resected tumors and confirmed by pathological review. Immunohistochemical staining was performed to assess the protein expression of NDRG2. NDRG2-overexpressed and knockdown HepG2/SMMC-7721 cell lines were infected by lentivirus and cultured, before measurement of glucose uptake, lactate production, lactase dehydrogenase activity, and oxygen consumption rate. NDRG2 and SIRT1 proteins were analyzed by western blot. Results: Both the mRNA and protein levels of NDRG2 as a tumor suppressor were downregulated in the liver tumors and the survival rate of patients negatively correlated with the expression of NDRG2. In the NDRG2-overexpressed and knockdown cell lines, NDRG2 showed inhibition of glycolysis in liver tumor cells. Our experimental data suggested the expression of SIRT1 negatively correlated with that of NDRG2. Conclusions: Our study findings enrich the understanding of the role of NDRG2 in tumor growth and of the mechanism by which NDRG2 regulates glycolysis. SIRT1, a deacetylase that plays an important role in glycolysis regulation, may be negatively regulated by NDRG2 in liver tumors.
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Registered trials
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