Evidence map›Paper›PMID 39387452›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Loss of Carbamoyl Phosphate Synthetase 1 Potentiates Hepatocellular Carcinoma Metastasis by Reducing Aspartate Level.

Siyuan Chen, Qin Tang, Manqiu Hu, Sijie Song, Xiaohong Wu, You Zhou, Zihan Yang, Siqi Liao, Li Zhou, Qingliang Wang and 6 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

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  13. Construction of a linezolid-resistant strain of methicillin-susceptibleFrontiers in cellular and infection microbiology · 2026
    Article
  14. Review
  15. Frontiers in nutrition · 2026
    Article
  16. Article
  17. Article
  18. 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

16 authors.

Siyuan ChenDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Qin TangDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Manqiu HuDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Sijie SongDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Xiaohong WuDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
You ZhouDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Zihan YangDepartment of Biomedical Sciences, and Tung Biomedical Sciences Center, City University of Hong Kong, 83 Tat Chee Avenue, Kowloon, Hong Kong SAR, 999077, P. R. China.
Siqi LiaoDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Li ZhouDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Qingliang WangDepartment of Pathology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Hongtao LiuDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Mengsu YangDepartment of Biomedical Sciences, and Tung Biomedical Sciences Center, City University of Hong Kong, 83 Tat Chee Avenue, Kowloon, Hong Kong SAR, 999077, P. R. China.
Zhe-Sheng ChenDepartment of Pharmaceutical Sciences, Institute for Biotechnology, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, 11439, USA.
Wei ZhaoSchool of Clinical Medicine, The First Affiliated Hospital, Chengdu Medical College, Sichuan, 610500, P. R. China.
Song HeDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Zhihang ZhouDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.ORCID 0000-0003-1356-9872

Funding

2.Chongqing Natural Science Foundation CSTB2022NSCQ-MSX07752.Chongqing Natural Science Foundation CSTB2022NSCQ-MSX10102.Chongqing Natural Science Foundation CSTB2022NSCQ-MSX1038Kuanren Talents Program of the Second Affiliated Hospital of Chongqing Medical University 13-004-009National Natural Science Foundation of China 82203791National Natural Science Foundation of China 8237300Natural Science Foundation of Chongqing Municipality CSTB2022NSCQ-MSX0775Natural Science Foundation of Chongqing Municipality CSTB2022NSCQ-MSX1010Natural Science Foundation of Chongqing Municipality CSTB2022NSCQ-MSX1038Open Project of Key Laboratory of Tumor Immunopathology, Ministry of Education 2020jsz604Senior Medical Talents Program of Chongqing for Young, and Middle-aged 13-004-009Young and Middle-aged Senior Medical Talents Studio of Chongqing
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide. Numerous studies have shown that metabolic reprogramming is crucial for the development of HCC. Carbamoyl phosphate synthase 1 (CPS1), a rate-limiting enzyme in urea cycle, is an abundant protein in normal hepatocytes, however, lacking systemic research in HCC. It is found that CPS1 is low-expressed in HCC tissues and circulating tumor cells, negatively correlated with HCC stage and prognosis. Further study reveals that CPS1 is a double-edged sword. On the one hand, it inhibits the activity of phosphatidylcholine-specific phospholipase C to block the biosynthesis of diacylglycerol (DAG), leading to the downregulation of the DAG/protein kinase C pathway to inhibit invasion and metastasis of cancer cells. On the other hand, CPS1 promotes cell proliferation by increasing intracellular S-adenosylmethionin to enhance the m6A modification of solute carrier family 1 member 3 mRNA, a key transporter for aspartate intake. Finally, CPS1 overexpressing adeno-associated virus can dampen HCC progression. Collectively, this results uncovered that CPS1 is a switch between HCC proliferation and metastasis by increasing intracellular aspartate level.

Indexed as

Carbamoyl-Phosphate Synthase (Ammonia)Carcinoma, HepatocellularLiver NeoplasmsAnimalsAspartic AcidCell Line, TumorCell ProliferationDisease Models, AnimalFemaleHumansMaleMiceMiddle AgedNeoplasm MetastasisAspartic AcidCarbamoyl-Phosphate Synthase (Ammonia)CPS1 protein, humanaspartateCPS1m6AmetastasisPC‐PLC

Identifiers

PMID39387452
PMCPMC11615744

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.