Evidence map›Paper›PMID 40514677›Full record

ArticleCancer cell international2025

Development of a circadian-related prognostic signature highlights RBM17 as a stemness regulator in liver cancer.

Jingsong Yan, Xiao Yang, Jiabin Lu, Shasha Wu, Yanchen Wang, Yuyang Du, Jingyi Zheng, Fenfen Wang, Han Gao, Hui Yang and 2 more

Abstract read
In one paragraph

Article in Cancer cell international, 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. Review
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

12 authors.

Jingsong Yan *Department of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Xiao Yang *Institute of Life Sciences, Chongqing Medical University, Chongqing, 400016, China.
Jiabin LuDepartment of Pathology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Shasha WuDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Yanchen WangShenzhen Hospital, Southern Medical University, Shenzhen, 518000, China.
Yuyang DuDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Jingyi ZhengShenzhen Hospital, Southern Medical University, Shenzhen, 518000, China.
Fenfen WangDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Han GaoDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Hui YangDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Shaoyan XiDepartment of Pathology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China. xishy@sysucc.org.cn.
Yan LiDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China. liyan181@smu.edu.cn.

Funding

Guangdong Provincial Natural Science Fund 2022A1515012284National Natural Science Foundation of China 82372768Shenzhen Science and Technology Innovation Commission JCYJ20220530115204011
6 · The paper itself

Abstract

The liver exhibits extensive circadian regulation among organs. Epidemiological studies have substantiated that disruptions in circadian rhythm constitute a risk factor for the oncogenesis of liver cancer. Nonetheless, the molecular underpinnings of how circadian dysregulation influences liver cancer progression remain elusive. Our research aims to elucidate these mechanisms and develop a predictive model for prognosis and treatment responsiveness. Our multi-omics analysis revealed extensive dysregulation of liver circadian genes (LCGs) in liver cancer. Employing machine learning algorithms, we pinpointed four pivotal dysregulated LCGs. Through the integration of single-cell, bulk, and spatial transcriptomics, we further elucidated the interconnections between LCGs dysregulation and the tumor microenvironment. In vivo and in vitro experiments demonstrated that RBM17, identified as a crucial dysregulated LCG, promotes the progression of liver cancer and cisplatin resistance by facilitating cancer stem cell phenotype. The circadian prognosis scores (CPS), based on these four genes, effectively reflected the prognosis of liver cancer patients and their responses to various therapeutic interventions. Mechanism of Action (MOA) analysis suggested that high CPS level may sensitize tumors to cell cycle-targeted therapies. Collectively, our findings provide new insights into the interplay between liver circadian gene regulation and liver cancer progression, and propose novel therapeutic targets for liver cancer.

Indexed as

BiomarkersCircadian genesLiver cancerRBM17

Identifiers

PMID40514677
PMCPMC12166579

What OpenQuestion holds

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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.