ArticleOncology letters2025
Targeting ETHE1 inhibits tumorigenesis
Article in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Harnessing glycolysis in gastric cancer: molecular targets, therapeutic strategies, and clinical horizons.Frontiers in immunology · 2025Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric adenocarcinoma (GAC) is a prevalent form of cancer that frequently displays abnormal metabolism characterized by increased aerobic glycolysis. Therefore, inhibition of glycolysis may exhibit therapeutic potential for the management of advanced or recurrent gastric cancer. Analysis of ethylmalonic encephalopathy protein 1 (ETHE1) expression levels in 30 pairs of cancerous and paracancerous tissues, and 50 tumor tissue sections collected from patients with GAC revealed that ETHE1 expression was upregulated in cancerous tissues compared with in paracancerous tissues. Advanced tumor stage, lymph node metastasis and Tumor-Node-Metastasis stage were associated with high ETHE1 expression. Knockdown of ETHE1 expression in GAC cells resulted in a significant inhibition of cell proliferation and in cell cycle arrest, accompanied by downregulated levels of cyclin D1 and cyclin-dependent kinase 4. ETHE1 knockdown also resulted in increased apoptosis of GAC cells, and increased caspase-3 and caspase-9 activity. Additionally, the expression levels of proteins associated with aerobic glycolysis were downregulated following ETHE1 knockdown, which may reduce glucose consumption, lactic acid production and ATP levels. In the
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