ArticleHuman mutation2026
Integrative Genomic Analysis Identifies MAGT1 as a Key Regulator of Proliferation and Poor Prognosis in Breast Cancer.
Article in Human mutation, 2026. 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Magnesium transporter 1 (MAGT1) plays a crucial role in magnesium homeostasis and immune regulation, yet its clinical significance and functional role in breast cancer remain largely unexplored. Methods: The expression pattern and prognostic value of MAGT1 in breast cancer were analyzed using data from The Cancer Genome Atlas (TCGA) and validated by immunohistochemistry on a tissue microarray comprising 60 patient samples. Genomic alteration analysis of MAGT1 with BRCA clinical implications was performed. The biological functions of MAGT1 were investigated in vitro using MCF-7 and MDA-MB-231 cell lines. MAGT1 expression was knocked down by siRNA, and its effects on cell proliferation, colony formation, DNA synthesis, migration, and invasion abilities were inhibited through MTT assays, colony formation assays, EdU assays, wound healing assays, and Transwell assays. Immune cell infiltration associated with MAGT1 expression was analyzed using bioinformatics tools. Results: MAGT1 was significantly overexpressed in breast cancer tissues compared with adjacent normal tissues. High MAGT1 expression was strongly associated with advanced tumor stage, poorer histological grade, and unfavorable patient prognosis, serving as an independent risk factor for overall survival. MAGT1 mutations were not statistically significantly associated with overall survival (OS) in breast cancer, but MAGT1 mutations were closely associated with ERBB2 and CDH1. Bioinformatic analysis revealed a correlation between MAGT1 expression and altered immune cell infiltration within the tumor microenvironment. In vitro functional assays demonstrated that silencing MAGT1 markedly inhibited the proliferative capacity, clonogenicity, migration, and invasion of breast cancer cells. Conclusion: Our findings indicate that MAGT1 is frequently upregulated in breast cancer and correlates with aggressive tumor behavior and poor clinical outcomes. MAGT1 promotes key oncogenic phenotypes in breast cancer cells and may influence the immune landscape, highlighting its potential as both a prognostic biomarker and a promising therapeutic target.
Indexed as
Identifiers
What Socratic 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 Socratic graph.