Evidence map›Paper›PMID 41550764›Full record

ArticleiScience2026

NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin.

Yumeng Wang, Xun Yang, Yihong Dong, Xinxin Yang, Yunjing Hou, Qiang Fu, Jun Yan, Yulu Du, Qingxin Zhang, Yunfei Zhou and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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.

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

18 authors.

Yumeng WangNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.
Xun YangNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.
Yihong DongNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.
Xinxin YangDepartment of Pathology, Harbin Medical University Cancer Hospital, Harbin, China.
Yunjing HouDepartment of Pathology, Harbin Medical University Cancer Hospital, Harbin, China.
Qiang FuBasic Medical College of Heilongjiang University of Chinese Medicine, Harbin, China.
Jun YanNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.
Yulu DuNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.
Qingxin ZhangNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.
Yunfei ZhouNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.
Aodi WuNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.
Shuyuan ChangNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.
Jianwen XuNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.
Chunhui ZhangDepartment of Student Affairs, The Fourth Hospital of Harbin Medical University, Harbin, China.
Xiaoyang HuBasic Medical College of Heilongjiang University of Chinese Medicine, Harbin, China.
Hongxue MengDepartment of Pathology, Harbin Medical University Cancer Hospital, Harbin, China.
Wei SunPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, Beijing, China.
Dabin LiuNHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy, The Fourth Hospital of Harbin Medical University, Harbin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a highly aggressive malignancy characterized by a paucity of therapeutic options. An analysis of multi-omics datasets, including The Cancer Genome Atlas (TCGA), the International Cancer Genome Consortium (ICGC), and the National Omics Data Encyclopedia (NODE) database, revealed that NAT10 is significantly upregulated in HCC and is associated with poor patient survival outcomes. Mechanistically, our findings demonstrate that NAT10 functions as an upstream activator of SQLE-dependent cholesterol biosynthesis via the AKT/mTOR signaling pathway. Additionally, as an RNA acetyltransferase, NAT10 enhances the stability of SQLE mRNA through ac4C modification, thereby revealing its dual synergistic role in promoting hepatocellular carcinogenesis. Both

Indexed as

Cell biologyMolecular biology

Identifiers

PMID41550764
PMCPMC12803925

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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.