ArticleCancer medicine2025
The Biological and Prognostic Implications of the Nicotinic Acetylcholine Receptor α3, α5, and α7 Subunits in Oral Squamous Cell Carcinoma.
Article in Cancer medicine, 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
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
1 citing paper in PubMed.
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
Abstract
backgroundThe divergent loop structures of nicotinic acetylcholine receptor (nAChR) α3, α5, and α7 subunits (encoded by CHRNA3, CHRNA5, and CHRNA7) are involved in kinase phosphorylation and signal transduction, potentially affecting oral squamous cell carcinoma (OSCC), the most common head and neck cancer (HNC). However, their specific roles in OSCC remain unclear.
methodsWe integrated analyses of SCC-4 tongue cancer cells with CHRNA overexpression, immunohistochemistry of OSCC pathological specimens, and data from the cancer genome atlas (TCGA), DepMap, and Puram 2017 to assess CHRNA3, CHRNA5, and CHRNA7 in OSCC/HNC.
resultsIn OSCC, CHRNA3, CHRNA5, and CHRNA7 expression interacted with epithelial-mesenchymal transition (EMT) markers and correlated with invasive patterns. CHRNA3 reduced epithelial and enhanced mesenchymal traits, supporting EMT. CHRNA5 further promoted mesenchymal features, was linked to disseminated tumor patterns, and predicted poor prognosis. CHRNA7 enhanced both epithelial and mesenchymal markers, maintaining a hybrid EMT state. In HNC, bioinformatic analyses revealed that CHRNA3 preserved ion channel activity, CHRNA5 promoted DNA replication, reduced adhesion, suppressed antigen presentation, and induced hypomethylation and miRNA overexpression, while CHRNA7 promoted differentiation with variable effects on adhesion and antigen presentation. In DepMap HNC cell lines, high CHRNA3/CHRNA5 and low CHRNA7 expression were associated with resistance to most inhibitors. Epidermal growth factor receptor (EGFR) inhibitors were effective in CHRNA3/CHRNA7-high HNC, whereas cyclin-dependent kinase (CDK) inhibitors were effective in CHRNA5-high HNC.
conclusionDifferential expression of CHRNA3, CHRNA5, and CHRNA7 indicates different EMT states in OSCC/HNC, influencing proliferation, differentiation, cell adhesion, immune reactions, and treatment efficacy, and warrants further experimental validation.
Indexed as
Identifiers
What 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.