ArticleCancer cell international2026
The NEAT1/miR-506-3p/STAT3 axis promotes uveal melanoma progression and represents a potential therapeutic target.
Article in Cancer cell international, 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
5 authors.
Funding
Abstract
Uveal melanoma (UM), a prevalent intraocular malignancy with a high rate of metastasis, particularly to the liver, presents a significant therapeutic challenge due to the absence of effective treatments. Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are under scrutiny for their roles in cancer, with lncRNA-NEAT1 identified as a key contributor to tumor growth. Our study delves into the aberrant expression of NEAT1, miR-506-3p, and STAT3 in UM cells compared with retinal pigment epithelial cells, revealing their impact on UM cell proliferation, migration, and invasion. Interventions targeting NEAT1 inhibition or miR-506-3p overexpression restrict UM cell viability, migration, and invasion. Conversely, increasing NEAT1 expression or suppressing miR-506-3p enhances these biological behaviors. Bioinformatic tools and dual-luciferase assays validated the specific binding of miR-506-3p to NEAT1 and its regulatory effect on STAT3. Rescue experiments further confirmed these interactions, contributing to a comprehensive understanding of the NEAT1/miR-506-3p/STAT3 axis in UM. The NEAT1/miR-506-3p/STAT3 axis has emerged as a promising diagnostic and therapeutic target for UM, providing a novel perspective on the pathogenesis of this challenging malignancy.
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.