ArticleMolecular therapy. Nucleic acids2026
Low circulating miR-5193 promotes PD-L1-mediated immune evasion and relates to immune checkpoint inhibitor response in esophageal cancer.
Article in Molecular therapy. Nucleic acids, 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
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low levels of circulating tumor-suppressor microRNAs are associated with cancer progression and poor prognosis. However, their role in immune evasion and response to immune checkpoint inhibitors (ICIs) remains unclear. We aimed to identify a PD-L1-targeting tumor-suppressor microRNA downregulated in esophageal squamous cell carcinoma (ESCC). Four tumor-suppressor microRNAs (miR-5193, miR-3117-3p, miR-802, and miR-651-3p) predicted to target programmed cell death ligand 1 (PD-L1) were selected. Plasma levels of miR-5193 were significantly lower in ESCC patients than in healthy volunteers. In 122 consecutive ESCC patients, low plasma miR-5193 was associated with advanced tumor depth and pathological stage and was an independent prognostic factor. In ESCC cells, miR-5193 suppressed PD-L1 expression. In a co-culture model of tumor cells and T cells, miR-5193 overexpression enhanced T cell antitumor activity by suppressing PD-L1. Among 56 ESCC patients treated with or without ICIs for recurrence, miR-5193 levels showed a trend toward an inverse association with PD-L1 tumor proportion score. In the low miR-5193 group, disease control rate was higher and ICI-treated patients showed a trend toward longer progression-free survival. Low levels of miR-5193 contribute to ESCC progression and poor outcomes and may serve as a biomarker reflecting tumor immune status and ICI-related outcomes.
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.