ArticleJournal of translational medicine2026
SMC4/SMAD3/NF-κB axis drives cervical cancer progression and radioresistance via DNA damage repair and immune modulation.
Article in Journal of translational medicine, 2026. 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.
- A three-gene radioresistance signature predicts tumor progression in cervical cancer.Translational cancer research · 2026Article
- Immune heterogeneity and therapeutic resistance in gynecological malignancies.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCervical cancer remains a significant global health burden, with the molecular determinants of its progression and therapeutic resistance not fully elucidated. This study aimed to identify DNA damage-related genes with prognostic and functional significance.
methodsFour cervical cancer GEO datasets were integrated and batch-corrected. Differential expression analysis and WGCNA were performed. Machine learning algorithms (LASSO, SVM, and Random Forest) were used to refine key genes. Functional roles of the pivotal gene SMC4 were investigated using in vitro experiments, including proliferation, colony formation, 3D spheroid assays, phalloidin staining, cell-cycle analysis, immunofluorescence, and analysis of DNA damage and immune-associated pathways under ionizing radiation.
resultsIntegration of transcriptomic data revealed 16 candidate genes. Machine learning convergence identified five core genes (CCNB2, CDKN2A, CHEK1, TYMS, and SMC4), all of which were significantly upregulated in tumors. Among these, SMC4 was uniquely associated with poor overall and disease-specific survival. Functional assays demonstrated that SMC4 knockdown under ionizing radiation significantly inhibited cervical cancer cell proliferation, colony formation, invasion, and reduced S-phase cells, and impaired DNA damage repair. Mechanistically, SMC4 was found to upregulate SMAD3, activate NF-κB signaling, and promote PD-L1 expression. Single-cell analysis confirmed SMC4's predominant expression in epithelial cells and its association with an altered tumor immune context.
conclusionOur study identifies SMC4 as a regulator that promotes radioresistance and potentially modulates the tumor immune microenvironment in cervical cancer, likely by coordinating DNA damage repair and activating the SMAD3-NF-κB pathway. These findings suggest that SMC4 could be a potential therapeutic target for radiosensitization and a candidate biomarker for patient stratification.
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.