ArticleBiochemical genetics2025
ETS1 Promotes Aerobic Glycolysis and Growth in Head and Neck Squamous Cell Carcinoma by Targeting RRAS2.
Article in Biochemical genetics, 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed.
- Genetic architecture of a Circadian Imbalance Index: genome-wide association, phenome-wide association, and Mendelian randomisation analyses.EBioMedicine · 2026Article
- Genome wide association study of a Circadian Imbalance Index in 312,935 European ancestry UK Biobank participants identifies loci related to diabetes, mood and myocardial infarction.Research square · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Head and neck squamous cell carcinoma (HNSCC) is a prevalent malignancy with a five-year survival rate below 50%, highlighting the urgent need for novel therapeutic targets. This study explores the role of the small GTPase RRAS2 in HNSCC progression and its regulation of glycolysis. Analysis of data from the TCGA and GTEx databases revealed that RRAS2 is significantly upregulated in HNSCC tissues and is associated with poorer overall patient survival. Functional experiments demonstrated that silencing RRAS2 in HNSCC cell lines inhibits glycolytic activity and cell proliferation while promoting apoptosis, whereas overexpression of RRAS2 enhances glycolysis and cell growth. Additionally, bioinformatics and experimental approaches identified the transcription factor ETS1 as an upstream regulator of RRAS2. ETS1 binds to the RRAS2 promoter, facilitating its transcription and contributing to metabolic reprogramming in HNSCC cells. Rescue experiments confirmed that the ETS1-RRAS2 axis is crucial for maintaining the glycolytic phenotype and proliferative capacity of HNSCC cells. These findings suggest that the ETS1-RRAS2 pathway plays a critical role in HNSCC progression and metabolic adaptation, positioning RRAS2 as a potential therapeutic target for improving patient outcomes.
Indexed as
Identifiers
39661306What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.