ArticleFrontiers in oncology2025
Role of SUV39H2 in shaping the malignant phenotype of triple-negative breast cancer.
Article in Frontiers in oncology, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: SUV39H2, a histone methyltransferase involved in H3K9 trimethylation and transcriptional silencing, has been implicated in cancer progression. However, its expression patterns, clinical relevance, and functional roles in various tumor types remain to be fully elucidated. Methods: SUV39H2 expression in multiple cancers and paired adjacent normal tissues was analyzed using the TCGA-GTEX database and Xiantao online tools. Prognostic significance was assessed by survival analysis. KEGG and GO enrichment analyses were conducted to explore potential functional roles. Immune infiltration correlations were evaluated based on TCGA data. Single-cell RNA sequencing from GSE176078 was analyzed for validation of expression patterns. Immunohistochemistry (IHC) was performed on five pairs of TNBC patient samples to confirm SUV39H2 expression. Western blotting (WB) was conducted to verify SUV39H2 knockdown efficiency in MDA-MB-231 and Hs-578T TNBC cells. Functional assays, including Transwell migration, colony formation, sphere formation, and subcutaneous xenograft tumorigenicity assays, were performed to evaluate the effects of SUV39H2 knockdown on TNBC cell growth and metastatic potential. Results: SUV39H2 was significantly overexpressed in multiple cancers, with consistently elevated levels in paired tumor-adjacent tissues. In TNBC, SUV39H2 expression was markedly upregulated across all clinical and TNM stages compared with normal tissues and other BRCA subtypes. Immunohistochemistry confirmed SUV39H2 overexpression in TNBC patient samples, and WB demonstrated successful knockdown in MDA-MB-231 and Hs-578T cells. Functional assays revealed that SUV39H2 knockdown significantly inhibited proliferation, migration, stemness, and Conclusions: SUV39H2 is consistently upregulated in triple-negative breast cancer and is associated with malignant features including enhanced proliferation, migration, stemness, and
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.