ArticleCommunications biology2025
Sema7a drives an immunosuppressive microenvironment of breast cancer via Kdm4a-mediated DNA replication regulation.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026Review
- Malignant B-cell States Orchestrate Spatially Organized Immune Ecosystems in B-cell Lymphomas.Research square · 2026Article
- Mitochondrial gene expression-based model for the prediction of thyroid cancer prognosis.Endocrine connections · 2026Article
- Comprehensive analysis of prognostic characteristics based on T cell-mediated tumor killing related genes in triple negative breast cancer.Frontiers in immunology · 2026Article
- Histone demethylase KDM4A promotes endometrial cancer progression through an ERRγ-associated cell-cycle regulatory axis.International journal of biological sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer remains a leading cause of cancer-related mortality worldwide, largely due to the persistence of an immunosuppressive tumor microenvironment that limits therapeutic efficacy. However, the molecular mechanisms underlying this immune suppression are not fully understood. Here, we identify Semaphorin 7 A (Sema7a) as a key regulator of antitumor immunity in breast cancer through its interaction with Lysine Demethylase 4 A (Kdm4a). Transcriptomic analyses of The Cancer Genome Atlas (TCGA) dataset revealed Sema7a as an immune-related hub gene using Weighted Gene Co-expression Network Analysis and Least Absolute Shrinkage and Selection Operator algorithms. Functional experiments in breast cancer cell lines demonstrated that loss of Sema7a reduced Kdm4a expression, induced DNA replication stress, and activated the cGAS-STING signaling pathway, thereby increasing IFN-β and CXCL10 secretion. These changes enhanced CD8⁺ T cell chemotaxis and cytotoxic activity, suppressing tumor growth and metastasis in vivo. Conversely, Kdm4a overexpression reversed the antitumor effects of Sema7a deficiency. Our findings establish the Sema7a-Kdm4a axis as a crucial mechanism shaping the immunosuppressive microenvironment in breast cancer and highlight its potential as a therapeutic target to enhance antitumor immunity.
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.