ArticleBMC cancer2025
DNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progression.
Article in BMC cancer, 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
6 authors.
Funding
Abstract
backgroundThe dysregulation of SOXs is related to tumor invasion, metastasis, proliferation, apoptosis, and epithelial-mesenchymal transition. This research sought to investigate the function and mechanisms of SOX21 in gastric cancer (GC).
methodsMultiple databases were included to determine the hub transcription factors in GC. In addition, RT-qPCR and Western blot were used to validate gene expression in tissues from GC patients. CCK-8, EdU, colony formation, wound healing, Transwell assays, and a xenograft tumor model were used to determine the function of SOX21 in GC. The targets of SOX21 were predicted and verified using ChIP, dual-luciferase reporter, and functional assays. SOX21 DNA methylation in GC cells was determined by qMSP. Rescue experiments were carried out in GC cells with DNMT1 silencing alone or in combination with SOX21 silencing.
resultsSOX21 was downregulated in GC tissues and cells. Ectopic expression of SOX21 inhibited cell growth, invasion, and migration, and induced apoptosis of GC cells. CKS2 was a target of SOX21, and overexpression of CKS2 promoted cell viability and mobility in GC cells overexpressing SOX21. The downregulation of SOX21 was related to the DNA hypermethylation catalyzed by DNMT1. The silencing of SOX21, by contrast, overturned the anti-tumor effects of sh-DNMT1 in vitro and in vivo.
conclusionOur data showed that DNMT1 overexpression upregulated CKS2 expression via hypermethylation of SOX21, thus promoting GC cell proliferation and growth, indicating that the DNMT1/SOX21/CKS2 axis could be a target for GC treatment.
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.