ArticleBiomolecules2025
LncRNA TSPEAR-AS2 Maintains the Stemness of Gastric Cancer Stem Cells by Regulating the miR-15a-5p/CCND1 Axis.
Article in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed.
- From epigenetics to metastasis: Multifaceted roles of lncRNAs in gastric cancer.Biochemistry and biophysics reports · 2026Review
- Advances in epigenetics of gastric cancer.Oncology reviews · 2026Review
- Dyskerin dysfunction in cancer development: from telomere dysregulation to immune deficiency.American journal of cancer research · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Cancer stem cells (CSCs), a subpopulation of tumor cells endowed with self-renewal capacity, drive cancer initiation and progression. While long non-coding RNAs (lncRNAs) are increasingly recognized as critical regulators of CSC stemness, their specific roles in gastric cancer stem cells (GCSCs) remain poorly understood. This study investigates the functional significance of lncRNA TSPEAR-AS2 in modulating GCSC properties and uncovers its underlying molecular mechanisms. Through integrated whole-transcriptome sequencing, bioinformatics analysis, and validation in 48 paired gastric cancer tissues and adjacent normal tissues, TSPEAR-AS2 was identified as a differentially expressed lncRNA upregulated in both GCSCs and tumor samples. Functional experiments revealed that TSPEAR-AS2 overexpression significantly enhanced GCSC sphere-forming ability, proliferation, cell cycle progression, epithelial-mesenchymal transition (EMT), and expression of stemness markers (CD54, CD44, OCT4, NANOG, and SOX2) while suppressing apoptosis. Conversely, TSPEAR-AS2 knockdown attenuated these malignant phenotypes. In vivo tumorigenicity assays in nude mice further confirmed that TSPEAR-AS2 promotes tumor growth, with overexpression accelerating and knockdown inhibiting tumor formation. Mechanistically, bioinformatics predictions and dual-luciferase reporter assays established TSPEAR-AS2 as a competing endogenous RNA (ceRNA) that sponges miR-15a-5p, thereby derepressing the miR-15a-5p target gene CCND1. Rescue experiments demonstrated that overexpression of miR-15a-5p phenocopied TSPEAR-AS2 knockdown, reducing GCSC stemness, while miR-15a-5p inhibition rescued the effects of TSPEAR-AS2 suppression. Collectively, these findings reveal a novel TSPEAR-AS2/miR-15a-5p/CCND1 regulatory axis that sustains GCSC stemness and tumorigenicity. These results highlight TSPEAR-AS2 as a potential therapeutic target for eradicating gastric cancer stem cells and improving clinical outcomes.
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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 OpenQuestion graph.