ArticleCellular and molecular life sciences : CMLS2026
Senescent epithelial cells remodel the tumor microenvironment and drive early LUAD progression: a multiomics risk model and single-cell analysis.
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. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Lung adenocarcinoma (LUAD) remains a major cause of cancer-related mortality, and there are currently few reliable biomarkers available for accurate prognosis and effective targeted therapy. Accumulating evidence demonstrates that senescent cells play an important role in tumor progression and immune evasion; nevertheless, their specific contribution to LUAD pathogenesis has not yet been fully elucidated. Accordingly, a five-gene senescence-related risk model comprising FGF2, GAPDH, CCNA2, ENO1, and DKK1 was established using the Least Absolute Shrinkage and Selection Operator regression applied to bulk RNA sequencing data obtained from The Cancer Genome Atlas (TCGA). Patients stratified as high risk by this model exhibited significantly poorer overall survival and progression-free survival, accompanied by marked activation of pathways associated with immune infiltration, epithelial–mesenchymal transition, and extracellular matrix remodeling. Integrative single-cell RNA sequencing analysis further revealed a distinct epithelial subpopulation (E9) defined by preferential activation of the senescence-associated gene DKK1. This subpopulation, which emerged from integrative single-cell transcriptomic analysis, exhibited pronounced senescence-associated characteristics, significantly increased cellular stemness, and extensive intercellular communication capacity, and uniquely expressed COL17A1 together with transcriptional programs that were strongly associated with epidermal development. Pseudotime analyses consistently positioned E9 cells at an early stage of tumor evolution. At the functional level, DKK1 contributed to senescence-associated phenotypic features, thereby promoting tumor cell migration and metastatic potential. From a clinical perspective, patients with concurrent high levels of COL17A1 and DKK1 expression experienced significantly worse clinical outcomes. Collectively, these findings identify a senescence-driven epithelial subpopulation that contributes to LUAD progression via DKK1-mediated activation of aging-related pathways and highlight DKK1 as a potential therapeutic target.
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.