Evidence map›Paper›PMID 38286671›Full record

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

Oxidative Stress Promotes Liver Cancer Metastasis via RNF25-Mediated E-Cadherin Protein Degradation.

Zhao Huang, Li Zhou, Jiufei Duan, Siyuan Qin, Jingwen Jiang, Haining Chen, Kui Wang, Rui Liu, Minlan Yuan, Xiangdong Tang and 4 more

Open access · goldAbstract 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 33 citations in OpenAlex.

  1. ADCY7 dictates N-cadherin stability to inhibit HCC metastasis.JHEP reports : innovation in hepatology · 2026
    Article
  2. Paving the Way to Elucidate Hg's Role in Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

14 authors at 5 institutions in 2 countries.

Zhao HuangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Li ZhouKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400016, China.
Jiufei DuanDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Siyuan QinDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Jingwen JiangWest China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, 610041, China.
Haining ChenColorectal Cancer Center, Department of General Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Kui WangWest China School of Basic Medical Sciences & Forensic Medicine, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Rui LiuState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Research Unit of Oral Carcinogenesis and Management, Chinese Academy of Medical Sciences, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China.
Minlan YuanMental Health Center and Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Biomedical Big Data Center, West China Hospital of Sichuan University, Chengdu, 610041, China.
Xiangdong TangSleep Medicine Center, Department of Respiratory and Critical Care Medicine, Mental Health Center, Translational Neuroscience Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Edouard C NiceDepartment of Biochemistry and Molecular Biology, Monash University, Clayton, VIC, 3167, Australia.
Yuquan WeiDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Wei ZhangFrontiers Medical Center, Tianfu Jincheng Laboratory, Chengdu, 610212, China.
Canhua HuangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.ORCID 0000-0003-2247-7750
Sichuan University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNDalian Medical University · CNMonash University · AUWest China Medical Center of Sichuan University · CN

Funding

1·3·5 project for disciplines of excellence, West China Hospital, Sichuan University ZYGD220071·3·5 project for disciplines of excellence, West China Hospital, Sichuan University ZYJC21004Ministry of Science and Technology of the People's Republic of China 2021ZD0201900National Key Research and Development Program of China 2020YFA0509400National Key Research and Development Program of China 2023YFC3402100National Natural Science Foundation of China 81821002National Natural Science Foundation of China 82103168National Natural Science Foundation of China 82130082National Natural Science Foundation of China 82341004
6 · The paper itself

Abstract

Loss of E-cadherin (ECAD) is required in tumor metastasis. Protein degradation of ECAD in response to oxidative stress is found in metastasis of hepatocellular carcinoma (HCC) and is independent of transcriptional repression as usually known. Mechanistically, protein kinase A (PKA) senses oxidative stress by redox modification in its β catalytic subunit (PRKACB) at Cys200 and Cys344. The activation of PKA kinase activity subsequently induces RNF25 phosphorylation at Ser450 to initiate RNF25-catalyzed degradation of ECAD. Functionally, RNF25 repression induces ECAD protein expression and inhibits HCC metastasis in vitro and in vivo. Altogether, these results indicate that RNF25 is a critical regulator of ECAD protein turnover, and PKA is a necessary redox sensor to enable this process. This study provides some mechanistic insight into how oxidative stress-induced ECAD degradation promotes tumor metastasis of HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsOxidative StressAntigens, CDCadherinsHumansProteolysisUbiquitin-Protein LigasesAntigens, CDCadherinsCDH1 protein, humanRNF25 protein, humanUbiquitin-Protein Ligasescancer metastasisoxidative stresspost‐translational modificationsredox signaling

Identifiers

PMID38286671
PMCPMC10987140
OpenAlexW4391329380

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.