ArticleBreast cancer research : BCR2023
The chromatin architectural regulator SND1 mediates metastasis in triple-negative breast cancer by promoting CDH1 gene methylation.
Article in Breast cancer research : BCR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 17 citations in OpenAlex.
- Computational Investigation of S781F Mutation-Induced Remodeling of the Staphylococcal Nuclease Domain-Containing Protein 1-Argonaute 2 Interface.International journal of molecular sciences · 2026Article
- Comparative Transcriptomics Suggests that Breast Secretory Epithelium Reuses Gene Repertoires Conserved Across Vertebrates Beyond Mammals.Genome biology and evolution · 2026Article
- Clonal evolution and stromal crosstalk drive an invasive epithelial program in bladder cancer.Frontiers in cell and developmental biology · 2026Article
- Mapping Non-Coding Epimutations in Breast Cancer: Advancing Epigenetics Towards Precision Medicine.Sub-cellular biochemistry · 2026Review
- Staphylococcal nuclease and tudor domain-containing protein 1: An emerging therapeutic target in cancer (Review).Molecular and clinical oncology · 2025Review
- Breaking the oncogenic alliance: advances in disrupting the MTDH-SND1 complex for cancer therapy.RSC advances · 2025Review
- Molecular targets of vortioxetine mediating glioblastoma suppression revealed by gene and protein network analyses and molecular docking simulations.The international journal of neuropsychopharmacology · 2025Article
- Recent advances on gene-related DNA methylation in cancer diagnosis, prognosis, and treatment: a clinical perspective.Clinical epigenetics · 2025Review
- The Valsa mali Effector VmSR1 Accelerates the Degradation of Tudor-SN2 to Suppress RNA Silencing and Plant Immunity.Molecular plant pathology · 2025Article
- Molecular profiling of breast cancer methylation pattern in triple negative versus non- triple negative breast cancer.Scientific reports · 2025Article
- The crosstalk between SND1 and PDCD4 is associated with chemoresistance of non-small cell lung carcinoma cells.Cell death discovery · 2025Article
- HMGA2 interacts with KAT6A to regulate MMPs chromatin architecture and promote triple-negative breast cancer metastasis.Frontiers in immunology · 2025Article
- Targeted therapy approaches for epithelial-mesenchymal transition in triple negative breast cancer.Frontiers in oncology · 2024Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSND1 participates in tumorigenesis, tumour invasion and metastasis in different cancers. Previous studies have shown that SND1 can promote the invasion and migration of breast cancer cells. Triple-negative breast cancer (TNBC) is a specific breast cancer subtype with high metastatic potential and poor prognosis. However, the specific roles and mechanisms of SND1 in TNBC metastasis remain unaddressed.
methodsImmunostaining was used to detect the SND1 expression in tissue samples of 58 TNBC and 10 glioblastomas (GBM) as positive control. The correlation between SND1 expression and patient prognosis was assessed using the Kaplan-Meier estimator. The gene expression was evaluated by qRT-PCR, Western blot and immunofluorescence analyses. Gene Ontology analysis, ChIP, a dual-luciferase reporter assay, EMSA, and 3C analysis were applied to identify SND1-activated target genes. Bisulfite sequencing PCR and MeDIP were used to detect DNA methylation. We also used wound healing, Transwell and orthotopic implantation assays to investigate the function of SND1 in TNBC cell migration and invasion.
resultsThe data of immunohistochemistry manifested that SND1 is the overexpression in metastasized TNBC and an independent factor for TNBC prognosis. SND1 knockdown inhibited the migration and invasion of TNBC cells. We found that SND1 promotes the metastatic phenotype of TNBC cells by epigenetically altering chromatin conformational interactions, which in turn activates DNMT3A transcription. Then, DNMT3A attenuates CCND1 expression by inducing CCND1 gene methylation, leading to TNBC metastasis.
conclusionSND1 can promote the invasion and migration of TNBC cells by promoting DNMT3A expression and suppressing CDH1 activity. SND1 is a potential biomarker and a promising therapeutic target for TNBC.
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.