Evidence map›Paper›PMID 41540504›Full record

ArticleBiomarker research2026

miR-22-Galectin-1 as an integral signaling axis in regulating metabolism and immunity in HCC.

Ying Hu, Tahereh Setayesh, Prasant Kumar Jena, Yutong Ji, Trenton Testerman, Ruiwu Liu, Tsung-Chieh Shih, Xiao-Jing Wang, Fu-Tong Liu, Kit S Lam and 1 more

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Article in Biomarker research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Ying Hu *Department of Pathology and Laboratory Medicine, University of California Davis, Sacramento, CA, USA.
Tahereh Setayesh *Department of Pathology and Laboratory Medicine, University of California Davis, Sacramento, CA, USA.
Prasant Kumar Jena *Department of Pediatrics, Cedars Sinai Medical Center, Los Angeles, CA, USA.
Yutong JiDepartment of Pathology and Laboratory Medicine, University of California Davis, Sacramento, CA, USA.
Trenton TestermanDepartment of Pathology and Laboratory Medicine, University of California Davis, Sacramento, CA, USA.
Ruiwu LiuDepartment of Biochemistry and Molecular Medicine, University of California Davis, Sacramento, CA, USA.
Tsung-Chieh ShihDepartment of Biochemistry and Molecular Medicine, University of California Davis, Sacramento, CA, USA.
Xiao-Jing WangDepartment of Pathology and Laboratory Medicine, University of California Davis, Sacramento, CA, USA.
Fu-Tong LiuDepartment of Dermatology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Kit S LamDepartment of Biochemistry and Molecular Medicine, University of California Davis, Sacramento, CA, USA.
Yu-Jui Yvonne WanDepartment of Pathology and Laboratory Medicine, University of California Davis, Sacramento, CA, USA. yjywan@health.ucdavis.edu.

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI KC KENT LLOYD · 2002 to 2026
$84.9M
Liver Cancer Therapy by MiR-22 and Its InducersR01CA222490 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WAN, YU-JUI YVONNE · 2018 to 2023
$2.1M
NCI NIH HHS P30 CA093373NCI NIH HHS R01 CA222490NIH HHS R01CA222490
6 · The paper itself

Abstract

backgroundWhile miR-22 is a suppressor of hepatocellular carcinoma (HCC), galectin-1 (Gal-1) serves as a HCC biomarker. Our previous studies have shown the effectiveness of miR-22 gene therapy and silencing Gal-1 as two potential novel options in treating HCC in preclinical mouse models. This study examines the significance of the miR-22-Gal-1 axis in HCC development and treatment.

methodsThe roles of miR-22 and Gal-1 in human HCC were analyzed using the Cancer Genome Atlas database based on their expression levels. The temporal effects of miR-22 were studied by analyzing signaling pathways affected by miR-22 expression levels during HCC progression. AAV8-miR-22, AAV9-Gal-1 siRNA, and LLS30, a Gal-1 inhibitor, were used to treat orthotopic mouse HCC. Spatial transcriptomics established the location-specific effects of miR-22 in mouse HCC. The signaling pathways affected by miR-22 and Gal-1 were identified by analyzing human HCC transcriptomics compared with those found in miR-22, Gal-1 siRNA, or LLS30-treated mouse HCC.

resultsIn the early stages of HCC, miR-22-high HCC exhibited extensive upregulation of endobiotic metabolism and xenobiotic detoxification signaling, accompanied by the activation of complement and clotting cascades. In late HCC stages, miR-22-high HCC exhibited heightened innate and adaptive immunity, associated with increased interferon signaling. These impacts were primarily observed in the tumors. At the tumor margin, miR-22 inhibited the Rho GTPase and cell-matrix interaction, revealing its role in reducing matrix remodeling and mobility. In non-tumor areas, miR-22 inhibited inflammation by reducing neutrophil degranulation, platelet activation, chemokine receptor binding, and fiber formation. miR-22, Gal-1 silencing, and LLS30 each exhibited anti-HCC effects and targeted common intracellular signaling pathways. Moreover, the anti-HCC effect of miR-22 was dependent on Gal-1 silencing. miR-22-high/Gal-1-low HCC patients had the best survival outcomes. In addition to the above-mentioned key intracellular pathways, miR-22 gene therapy and Gal-1 siRNA treatment of HCC reduced O-linked glycosylation, suggesting the role of the miR-22-Gal-1 axis in modifying glycosylation, which may affect the extracellular functions of Gal-1.

conclusionIn summary, the miR-22-Gal-1 axis can be an HCC prognostic biomarker, and it has vital roles in regulating metabolism and tumor immunity.

Indexed as

ComplementGlycanImmunityLiverRho GTPase

Identifiers

PMID41540504
PMCPMC12809943

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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.