ArticleiScience2026
LncRNA SLC16A1-AS1 cooperates with NSUN2 to stabilize GRP78 mRNA via m5C modification in gastric cancer.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- GRP78 dysregulation: A proposed molecular mechanism linking the tumor microenvironment to sepsis susceptibility in patients with cancer (Review).International journal of molecular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNAs (lncRNAs) play crucial roles in regulating chromatin dynamics and gene expression, and their dysregulation is closely linked to tumorigenesis. However, their specific functions in gastric cancer (GC) remain poorly understood. Here, we found that lncRNA solute carrier family 16 member 1 antisense RNA 1 (SLC16A1-AS1) was markedly overexpressed in GC through integrated RNA sequencing (RNA-seq) analysis and validation in clinical tissues. High SLC16A1-AS1 expression correlated with advanced cancer stage, greater invasion depth, and poorer patient prognosis. Functional assays showed that SLC16A1-AS1 overexpression promoted GC cell proliferation, whereas knockdown inhibited proliferation
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.