Evidence map›Paper›PMID 41160272›Full record

ArticleDiscover oncology2025

CENP-F promotes HCC cell proliferation mediated by super enhancer reader BRD4.

Yunhui Liu, Wenjiao Chen, Yuxin Niu, Xiaoqin Dong, Jie You, Zhongyuan Yang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
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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

6 authors.

Yunhui Liu *Department of Infectious Diseases, Tongji Hospital, Tongji Medical College, State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, Hubei, People's Republic of China.
Wenjiao Chen *Department of Dermatology, Wuhan Hankou Hospital, Wuhan, Hubei, China.
Yuxin NiuDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College, State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, Hubei, People's Republic of China.
Xiaoqin DongDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College, State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, Hubei, People's Republic of China.
Jie YouDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College, State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, Hubei, People's Republic of China.
Zhongyuan Yang *Department of Infectious Diseases, Tongji Hospital, Tongji Medical College, State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, Hubei, People's Republic of China. 1049446560@qq.com.

Funding

the Provincial Natural Science Foundation Innovation and Development Joint Fund Project of Hubei 2024AFD447
6 · The paper itself

Abstract

Centromere protein F (CENP-F) is highly expressed in hepatocellular carcinoma (HCC), but the specific mechanism by which it regulates the occurrence and development of HCC is currently unclear. The activities of the super enhancer (SE) readers bromodomain-containing protein 4 (BRD4), cyclin-dependent kinase 1 (CDK1), cyclin-dependent kinase 2 (CDK2) and cyclin-dependent kinase 7 (CDK7) are significantly increased in HCC. This study explored the mechanism of CENP-F regulation in HCC through bioinformatics and cell and animal experiments. We found that the protein levels of CENP-F, CDK1, CDK2, CDK7 and BRD4 were significantly increased in HCC and that CENP-F was closely associated with CDK1, CDK2, CDK7 and BRD4. Downregulation of CENP-F led to a decrease in the protein levels of CENP-F, CDK1, CDK2, BRD4 and c-Myc and inhibited the proliferation of HepG2 and Hep3B cells. After overexpression of CENP-F, the above parameters returned to their previous levels. In addition, downregulation of BRD4 using siRNA and JQ1 led to decreases in the protein levels of BRD4 and c-Myc. CENP-F or BRD4 knockdown inhibited xenograft tumor growth in an in vivo HCC model. These findings suggested that CENP-F regulated the proliferation of HCC cells through the CENP-F-CDK1/CDK2-BRD4 axis. In conclusion, our study revealed a new mechanism by which CENP-F promotes HCC cell proliferation by the SE reader BRD4, suggesting that SEs play an essential role in mediating HCC treatment.

Indexed as

Bromodomain-containing protein 4Centromere protein fHepatocellular carcinomaSuper enhancerTreatment

Identifiers

PMID41160272
PMCPMC12572522

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.