Evidence map›Paper›PMID 40883414›Full record

ArticleOncogene2025

RBM30 recruits DOT1L to activate STAT1 transcription and drive immune evasion in hepatocellular carcinoma.

Hexu Han, Chen Gong, Yue Zhang, Cuixia Liu, Yifan Wang, Dakun Zhao, Junxing Huang, Zhicheng Gong

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

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  15. Frontiers in immunology · 2026
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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

8 authors.

Hexu Han *Department of Gastroenterology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, Jiangsu, China. 1920716577@qq.com.ORCID 0000-0002-5812-0123
Chen Gong *Department of Gastroenterology, Taicang Affiliated Hospital of Soochow University, The First People's Hospital of Taicang, Taicang, Jiangsu Province, China.
Yue Zhang *Clinical Medical Laboratory Center, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou, Jiangsu, China.
Cuixia Liu *Department of Gastroenterology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, Jiangsu, China.
Yifan WangDepartment of Gastroenterology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, Jiangsu, China.
Dakun ZhaoDepartment of Gastroenterology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, Jiangsu, China.
Junxing HuangDepartment of Oncology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, Jiangsu, China. hjxtz@sina.cn.ORCID 0009-0000-7728-4126
Zhicheng GongWuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China. 9862021019@jiangnan.edu.cn.

Funding

Nanjing Medical University (NMU) TZKY20240109
6 · The paper itself

Abstract

Programmed death ligand 1 (PD-L1) is a protein expressed in hepatocellular carcinoma (HCC) that drives immune evasion by binding to programmed death receptor 1 (PD-1) on activated T cells. Understanding PD-L1 regulation is essential to understand the immunosuppressive microenvironment for antitumor immunity. We screened ribonucleic acid (RNA)-binding motif proteins (RBMs). RBM30 can enhance PD-L1 expression in HCC cells. In this study, we found that high RBM30 expression in tumor tissues can drive HCC tumor immune evasion and accelerate disease progression via increased PD-L1 transcription. We conducted multiple molecular and high-throughput assays to elucidate the intrinsic molecular mechanisms by which RBM30 upregulates PD-L1 expression in HCC. RBM30 binds to DNA near the transcriptional start site of STAT1 and recruits DOT1L to promote H3K79me3 enrichment, enhancing its accessibility to upregulate STAT1 transcription, consequently activating the PD-L1 transcription. This enhances PD-L1 expression to facilitate immune evasion. These findings reveal the vital role of RBM30 in HCC immune evasion.

Indexed as

Carcinoma, HepatocellularImmune EvasionLiver NeoplasmsRNA-Binding ProteinsSTAT1 Transcription FactorTumor EscapeAnimalsB7-H1 AntigenCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceTranscription, GeneticB7-H1 AntigenCD274 protein, humanRNA-Binding ProteinsSTAT1 protein, humanSTAT1 Transcription Factor

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Registered trials

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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.