ArticleCellular and molecular life sciences : CMLS2026
HOXC6 overexpression stimulates cell migration and correlates with poor prognosis in head and neck squamous cell carcinoma.
Article in Cellular and molecular life sciences : CMLS, 2026. 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.
- HOX gene dysregulation in head and neck squamous cell carcinoma: mechanisms, clinical relevance, and future perspectives.Frontiers in oncology · 2026Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide and accounts for 2% of cancer-related deaths. Although the oncogenic role of HOXC6 in solid tumors is known, its functional relevance in HNSCC remains elusive. Using The Cancer Genome Atlas (TCGA, with 520 HNSCC samples) data and in vitro models, we investigated the functional role of HOXC6 in HNSCC. TCGA analysis revealed that HOXC6 overexpression in HNSCC tissues correlated with malignant progression and poor survival outcomes. In vitro studies confirmed HOXC6 overexpression in HNSCC cell lines, and knockdown of HOXC6 significantly reduced both cell proliferation and migration, highlighting the oncogenic role of HOXC6. Additionally, pathway analysis of RNA-seq data linked HOXC6 expression with immune evasion and dysregulation of cell cycle genes, particularly the E2F and G2M checkpoints. Furthermore, H3K27ac ChIP-seq data showed that histone acetylation at the HOXC6 promoter drives HOXC6 overexpression. This study identified HOXC6 as a key oncogenic driver in HNSCC and as a candidate biomarker for HNSCC. Targeting HOXC6 could pave the way for improved biomarker-driven approaches in HNSCC treatment to reduce recurrence and improve patient survival rates.
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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.