Evidence mapPaperPMID 41450464Full record

ArticleFrontiers in genetics2025

Adrenomedullin orchestrates treatment resistance in hepatocellular carcinoma via immune microenvironment remodeling.

Xixi Gao, Yongliang Sun, Jia Huang, Li Xu, Hanchun Huang, Zhiying Yang

Abstract read
In one paragraph

Article in Frontiers in genetics, 2025. 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. Article
4 · The record

Corrections and comments

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

6 authors.

Xixi GaoChina-Japan Friendship Hospital, Beijing, China.
Yongliang SunChina-Japan Friendship Hospital, Beijing, China.
Jia HuangChina-Japan Friendship Hospital, Beijing, China.
Li XuChina-Japan Friendship Hospital, Beijing, China.
Hanchun HuangChina-Japan Friendship Hospital, Beijing, China.
Zhiying YangChina-Japan Friendship Hospital, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Hepatocellular carcinoma (HCC) displays marked cellular heterogeneity and immune microenvironment complexity that fundamentally influence transcatheter arterial chemoembolization (TACE) treatment responses and patient outcomes. Deciphering the molecular architecture underlying therapy resistance remains essential for advancing precision oncology in HCC management. Methods: We integrated four single-cell RNA sequencing cohorts with bulk transcriptomic datasets and longitudinal clinical annotations from The Cancer Genome Atlas Liver Hepatocellular Carcinoma database and Gene Expression Omnibus repositories to perform multidimensional analyses. Computational frameworks including single-cell Phenotype Associated Score (scPAS), high-dimensional weighted gene co-expression network analysis (hdWGCNA), and Single-Cell Regulatory Network Inference and Clustering (SCENIC) were deployed to identify resistance-linked cellular subpopulations and pivotal regulatory modules. Functional validation employed adrenomedullin (ADM)-depleted Huh7 cellular models and xenograft tumor-bearing mouse systems, with mechanistic interrogation via Western immunoblotting, quantitative reverse transcription polymerase chain reaction, and Kaplan-Meier survival estimation to confirm ADM biological functions and clinical relevance. Results: We identified a TACE-resistant malignant cell subset (scPAS+) characterized by pronounced activation of glycolytic, hypoxic, and epithelial-mesenchymal transition pathways alongside overexpression of resistance-conferring genes including LINC00221, hexokinase 2, and alpha-fetoprotein. This cellular phenotype demonstrated robust associations with TACE non-responsiveness, sorafenib cross-resistance, and abbreviated patient survival. Patient stratification based on scPAS + signature genes delineated two distinct molecular subgroups: the scPAS + -enriched cohort exhibited marked TACE refractoriness, elevated sorafenib failure rates, immunosuppressive microenvironmental architecture, and diminished 5-year survival probability. Mechanistic investigations established ADM as a critical driver orchestrating this resistance phenotype. ADM depletion attenuated Huh7 cell proliferative capacity, migratory potential, and invasive behavior, reduced xenograft tumor burden in murine models, and substantially potentiated sorafenib antitumor efficacy. Conclusion: This study delineates an ADM-driven TACE-resistant HCC cellular subtype (scPAS+) that functions simultaneously as a prognostic biomarker and actionable therapeutic target for circumventing treatment resistance.

Indexed as

adrenomedullinhepatocellular carcinomasingle-cell RNA sequencingsorafenibtranscatheter arterial chemoembolizationtumor immune microenvironment

Identifiers

PMID41450464
PMCPMC12736389

What Socratic holds

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Registered trials

None linked

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.