ArticleDiscover oncology2025
CER1 as a manganese ion metabolism gene drives gastric cancer progression and therapeutic potential via oxidative stress and tumor microenvironment regulation.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Abstract
backgroundMetal ions are vital for biological regulation and contribute to gastric cancer (GC) development, but the mechanisms are unclear. This study investigates the role of the manganese ion metabolism (MIM)-related gene CER1 in GC, focusing on how CER1 induces oxidative stress, contributes to tumor microenvironment heterogeneity, and its potential for targeted personalized therapy.
methodsUsing single-cell RNA sequencing and multi-omics technologies, we characterized molecular subtypes of gastric cancer (GC) and explored the biological roles of the MIM family, elucidating genetic mechanisms of GC initiation and immune dysregulation.
resultsOur analysis systematically clarified the pivotal role of the MIM gene family in GC, and revealed that CER1 promoted T cell exhaustion and facilitated immune evasion. The bioinformatics analysis indicated that CER1 may regulate tumor cell biological behavior through the NRF2/KEAP1-mediated oxidative stress signaling pathway. In summary, CER1, as a member of the MIM family, serves as a central hub in the oxidative stress and immune regulation.
conclusionThe in-depth investigation of CER1 within the MIM family has markedly deepened our understanding of the complex molecular mechanisms underlying GC. Through targeted manipulation of the NRF2/KEAP1 oxidative stress pathway and T cell function, CER1 emerges as a strategic pathway for potentially inhibiting tumor growth. This investigation outlines a strategic framework to facilitate the advancement of innovative treatment modalities.
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.