ArticleHeliyon2023
The roles and molecular mechanisms of long non-coding RNA WT1-AS in the maintenance and development of gastric cancer stem cells.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Spheroids and organoids to study long noncoding RNAs in cancer: how they could replace animal models.Cancer metastasis reviews · 2026Review
- WT1-AS acts as a tumor suppressor in cervical cancer via OSR2-mediated transcriptional activation.Translational cancer research · 2026Article
- The WT 1-AS/miR-206 axis regulates the proliferation and migration of breast cancer through the cuproptosis related geneTranslational cancer research · 2026Article
- Serine metabolism reprogramming in cancer: a multi-tiered regulatory framework.Acta biochimica et biophysica Sinica · 2025Review
- Non-coding RNAs in gastric cancer: mechanisms and therapeutic prospects.Molecular cancer · 2025Review
- Epigenetic crosstalk between stem cells and tumors: mechanisms and emerging perspectives.American journal of stem cells · 2025Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been proposed that cancer stem cells (CSCs) are responsible for almost all malignant phenotypes of tumors. Long non-coding RNA WT1 antisense RNA (WT1-AS) has been found to be implicated in lung cancer cell stemness. However, the roles and molecular mechanisms of WT1-AS in the development of gastric cancer stem cells (GCSCs) remain unknown. Our present study showed that WT1-AS negatively regulated WT1 expression in GCSCs. WT1-AS knockdown or Wilms' tumor 1 (WT1) overexpression improved GCSC proliferative and migratory capacities, inhibited GCSC apoptosis, potentiated the resistance of GCSCs to 5-FU, promoted GCSC EMT, induced HUVEC angiogenesis, enhanced GCSC stemness, and facilitated
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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.