Evidence map›Paper›PMID 37880213›Full record

ArticleCell death discovery2023

ZNF281 inhibits mitochondrial biogenesis to facilitate metastasis of hepatocellular carcinoma.

Qingfang Zhao, Chenguang Zhang, Xialu Zhang, Shanshan Wang, Ting Guo, Yuzhe Yin, Hui Zhang, Zhuo Li, Yang Si, Yabin Lu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026
    Review
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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

12 authors at 4 institutions in 1 country.

Qingfang Zhao *School of Basic Medical Sciences, Capital Medical University, Beijing, 100069, China.ORCID http://orcid.org/0000-0002-2740-967X
Chenguang Zhang *School of Basic Medical Sciences, Capital Medical University, Beijing, 100069, China. chzhang@ccmu.edu.cn.ORCID http://orcid.org/0000-0003-4093-9322
Xialu ZhangSchool of Basic Medical Sciences, Capital Medical University, Beijing, 100069, China.
Shanshan WangBeijing Institute of Hepatology, Beijing You' An Hospital, Capital Medical University, Beijing, 100069, China.
Ting GuoKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Division of Gastrointestinal Cancer Translational Research Laboratory, Peking University Cancer Hospital & Institute, Beijing, 100142, China.
Yuzhe YinThe Sixth Clinical Medical School, Capital Medical University, Beijing, 100069, China.
Hui ZhangState Key Laboratory of Membrane Biology, School of Life Sciences, Tsinghua University, Beijing, 100084, China.
Zhuo LiDepartment of Pathology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China.
Yang SiSchool of Basic Medical Sciences, Capital Medical University, Beijing, 100069, China.
Yabin LuSchool of Basic Medical Sciences, Capital Medical University, Beijing, 100069, China.
Shan ChengSchool of Basic Medical Sciences, Capital Medical University, Beijing, 100069, China.ORCID http://orcid.org/0000-0002-8658-6916
Wei DingSchool of Basic Medical Sciences, Capital Medical University, Beijing, 100069, China. weiding@ccmu.edu.cn.ORCID http://orcid.org/0000-0002-1664-3401
Capital Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CNTsinghua University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82071235Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation) 7222001
6 · The paper itself

Abstract

Zinc finger protein 281 (ZNF281) has been shown to promote tumor progression. However, the underlying mechanism remains to be further elucidated. In this study, ZNF281 knockdown increased the expression of mitochondrial transcription factor A (TFAM) in hepatocellular carcinoma (HCC) cells, accompanied with increment of mitochondrial content, oxygen consumption rate (OCR) and levels of TCA cycle intermetabolites. Mechanistic investigation revealed that ZNF281 suppressed the transcription of TFAM, nuclear respiratory factor 1 (NRF1) and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). Furthermore, ZNF281 interacted with NRF1 and PGC-1α, and was recruited onto the promoter regions of TFAM, TFB1M and TFB2M repressing their expression. Knockdown of TFAM reversed ZNF281 depletion induced up-regulation of mitochondrial biogenesis and function, as well as impaired epithelial mesenchymal transition, invasion and metastasis of HCC cells. Our research uncovered a novel suppressive function of ZNF281 on mitochondrial biogenesis through inhibition of the NRF1/PGC-1α-TFAM axis, which may hold therapeutic potentials for HCC.

Identifiers

PMID37880213
PMCPMC10600106
OpenAlexW4387938539

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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.