ArticleBMC cancer2025
Single-cell sequencing reveals the role of SALL4 in cervical cancer development.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Advancements in single-cell sequencing for cervical cancer research.Molecular and cellular biochemistry · 2026Review
- Identification of malignant cells in single-cell transcriptomics data.Communications biology · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aims to investigate the role of SALL4 in the development and progression of cervical cancer, particularly its impact on the proliferation, migration and adhesion of HeLa cells, and to explore the clinical potential of SALL4 as a therapeutic target.
methodsSingle-cell sequencing technology was utilized to analyze the cellular characteristics of cervical cancer tumor cell populations, and transcriptomic data were integrated to assess the differential expression of SALL4. Additionally, both in vitro and in vivo experiments were conducted to evaluate the effects of SALL4 inhibition on cell proliferation, migration, adhesion, and its regulation of collagen content and fibrosis.
resultsHigh expression of SALL4 significantly promoted the proliferation, migration, and adhesion of cervical cancer cells. After SALL4 knockout, the migration and proliferation rates were significantly lower than those of HeLa cells. Immunofluorescence and in vivo experiments showed that SALL4 knockout cells exhibited a significantly reduced tumor formation ability, with lower proliferation and fibrosis levels compared to HeLa cells.
conclusionHigh expression of SALL4 promotes cervical cancer progression, while inhibition of SALL4 expression effectively suppresses cancer development. As a critical regulatory factor, SALL4 has the potential to become a therapeutic target for cervical cancer, and its application in cervical cancer treatment warrants further exploration.
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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.