Evidence map›Paper›PMID 41339318›Full record

ArticleCell death discovery2025

Aurora-A-mediated cytosolic localization of Maf1 promotes cell proliferation via regulating mitochondrial function in HCC.

Shiang-Jie Yang, Yu-Heng Kuan, Zong-Xin Ooi, Hong-Sheng Lai, Hsin-Yi Wu, Pao-Chi Liao, Yih-Jyh Lin, Che Min Su, Ming-Derg Lai, Liang-Yi Hung

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Shiang-Jie Yang *The Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Yu-Heng Kuan *Department of Biotechnology and Bioindustry Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, 70101, Taiwan.
Zong-Xin OoiDepartment of Biotechnology and Bioindustry Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, 70101, Taiwan.
Hong-Sheng LaiDepartment of Biotechnology and Bioindustry Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, 70101, Taiwan.
Hsin-Yi WuInstrumentation Center, National Taiwan University, Taipei, 106, Taiwan.
Pao-Chi LiaoDepartment of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, Tainan, 704, Taiwan.
Yih-Jyh LinDepartment of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Che Min SuDepartment of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Ming-Derg LaiThe Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Liang-Yi HungThe Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan. lyhung@mail.ncku.edu.tw.ORCID http://orcid.org/0000-0002-7284-2608

Funding

Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) MOST-111-2320-B-006-026National Cheng Kung University Hospital (NCKU Hospital) NCKUH-11302051National Cheng Kung University Hospital (NCKU Hospital) NCKUH-11302064National Cheng Kung University Hospital (NCKU Hospital) NCKUH-11402013National Cheng Kung University Hospital (NCKU Hospital) NCKUH-11402017
6 · The paper itself

Abstract

Maf1 is a well-known RNA polymerase III repressor and functions as a tumor suppressor due to its role in inhibiting tRNA synthesis. However, the role of Maf1 in hepatocellular carcinoma (HCC) remains unclear. This study identified Aurora-A as a novel upstream regulator of Maf1 in HCC. We demonstrated that Aurora-A interacts with the C domain of Maf1 and phosphorylates it at Threonine-212, leading to increased protein stability and cytosolic accumulation of Maf1. Importantly, the Aurora-A-enhanced cytosolic localization of Maf1 promotes mitochondrial dysfunction and glycolytic activity, ultimately driving HCC cell proliferation. In contrast, mutation of the Thr-212 site abolishes these effects, confirming its critical role. Significantly, elevated Maf-1 expression correlates with unfavorable clinical outcomes in HCC, particularly among patients with high Aurora-A expression. Furthermore, HCC cells with overexpressed Maf1 have heightened sensitivity to Aurora-A inhibitors, suggesting a potential therapeutic vulnerability. Our study uncovers a non-canonical, oncogenic role of Maf1 in HCC and highlights the Aurora-A-Maf1 axis as a promising target for personalized cancer therapy.

Identifiers

PMID41339318
PMCPMC12717421

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.