ArticleBMC cancer2023
ESCO2 promotes hypopharyngeal carcinoma progression in a STAT1-dependent manner.
Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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
4 citing papers in PubMed, 6 citations in OpenAlex.
- Carcinogenic role of ESCO2 in cholangiocarcinoma: integration of bioinformatics analysis and experimental validation.Translational cancer research · 2026Article
- Discovery and validation of proliferative exhausted T cells as a favorable prognostic biomarker in esophageal squamous cell carcinoma.Scientific reports · 2025Article
- The expression of establishment of cohesion 1 homolog 2 (ESCO2) in tumor cells and its research progress as a therapeutic target.European journal of medical research · 2025Review
- ESCO2 inhibition induces cell cycle arrest and apoptosis in breast cancer via the P53-CDK1 axis and the BAX/Bcl2/caspase signaling cascade.Frontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe establishment of sister chromatid cohesion N-acetyltransferase 2 (ESCO2) is involved in the development of multiple malignancies. However, its role in hypopharyngeal carcinoma (HPC) progression remains uncharacterized.
methodsThis study employed bioinformatics to determine the ESCO2 expression in head and neck squamous cell carcinoma (HNSC) and normal tissues. In vitro cell proliferation, migration, apoptosis, and/or cell cycle distribution assays were used to determine the function of ESCO2 and its relationship with STAT1. Xenograft models were established in nude mice to determine ESCO2 in HPC growth in vivo. Co-immunoprecipitation/mass spectrometry (Co-IP/MS) was conducted to identify the potential ESCO2 binding partners.
resultsWe found that ESCO2 expression was elevated in HNSC tissues, and ESCO2 depletion suppressed tumor cell migration in vitro and inhibited tumor growth in vitro and in vivo. Co-IP/MS and immunoblotting assays revealed the interaction between ESCO2 and STAT1 in HPC cells. STAT1-overexpression compromised ESCO2-mediated suppressive effects on HPC cell proliferation, viability, and migration.
conclusionsThese findings suggest that ESCO2 is crucial in promoting HPC malignant progression through the STAT1 pathway and provides novel therapeutic targets for HPC treatment.
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