ArticleJournal of cancer research and clinical oncology2026
The GC-derived exosomal LncRNA DARS-AS1 activates Wnt/β-catenin pathway to drive angiogenesis by regulating miR-605-5p/BCL9.
Article in Journal of cancer research and clinical oncology, 2026. 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
7 authors.
Funding
Abstract
backgroundGastric cancer (GC) is one of the most prevalent and aggressive malignancies globally, characterized by high morbidity and mortality rates despite advancements in medical technologies and screening methods. Recent studies have suggested that long non-coding RNAs (lncRNAs), particularly aspartyl-tRNA synthetase antisense RNA 1 (DARS-AS1), may play significant roles in tumor progression; however, its specific function in GC remains unclear. Therefore, this study aimed to clarify the contribution of DARS-AS1 to the progression and prognosis of GC.
methodsWe utilized quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC) to assess DARS-AS1 and CD31 expression levels in GC tissues derived from various cohorts. Additionally, functional studies involving knockdown of DARS-AS1 in GC cells were conducted to evaluate the effects on migration and angiogenesis in human umbilical vein endothelial cells (HUVECs) mediated by exosomes.
resultsOur analyses revealed that DARS-AS1 is significantly upregulated in GC tissues and is associated with malignant progression and poor prognosis. Furthermore, elevated DARS-AS1 levels correlated positively with tumor microvessel density (MVD). The knockdown of DARS-AS1 resulted in decreased migration and tube-forming ability of HUVECs in vitro. Mechanistically, we demonstrated that the exosomal transfer of DARS-AS1 from GC cells activates the Wnt/β-catenin signaling pathway by targeting miR-605-5p, thus promoting angiogenesis.
conclusionOur findings highlight the pivotal role of DARS-AS1 in enhancing GC progression through the activation of angiogenesis via the Wnt signaling pathway. By elucidating the mechanism underlying DARS-AS1-mediated tumorigenesis, we posit that DARS-AS1 could serve as a prognostic biomarker and a potential therapeutic target for GC intervention, warranting further exploration in clinical settings.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.