Evidence map›Paper›PMID 37156912›Full record

ArticleNature cell biology2023

Creatine kinase B suppresses ferroptosis by phosphorylating GPX4 through a moonlighting function.

Ke Wu, Meisi Yan, Tong Liu, Zheng Wang, Yuran Duan, Yan Xia, Guimei Ji, Yuli Shen, Lei Wang, Lin Li and 16 more

Abstract read
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In one paragraph

Article in Nature cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
41.1field-weighted citation impact, top 1% 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

118 citing papers in PubMed, 159 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Review
  9. GLS1 Orchestrates Exosome-Mediated Tumor-Endothelial Communication to Facilitate Angiogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  10. Article
  11. Macrophage Extracellular Traps in Immunity and Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  12. Review
  13. Crosstalk between autophagy and ferroptosis in liver diseases (Review).International journal of molecular medicine · 2026
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. HPD is an mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  20. Article

58 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

26 authors at 5 institutions in 2 countries.

Ke Wu *Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Meisi Yan *School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Tong Liu *Department of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.ORCID http://orcid.org/0000-0001-9234-1328
Zheng Wang *Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Yuran DuanZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Yan XiaDepartment of Cancer Biology, Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Guimei JiZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Yuli ShenZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Lei WangZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Lin LiZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Peixiang ZhengZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Bofei DongZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Qingang WuZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Liwei XiaoZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Xueying YangCancer Center, Zhejiang University, Hangzhou, China.
Haochen ShenZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Ting WenZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Jingjing ZhangZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
Jinfeng YiSchool of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Yuhan DengDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Xu QianDepartment of Clinical Laboratory, Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, China.
Leina MaThe Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.ORCID http://orcid.org/0000-0003-3964-632X
Jing FangThe Affiliated Hospital of Qingdao University and Qingdao Cancer Institute, Qingdao, China.
Qin ZhouSchool of Basic Medical Sciences, Harbin Medical University, Harbin, China. zhouqin@hrbmu.edu.cn.ORCID http://orcid.org/0000-0003-3879-4021
Zhimin LuZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China. zhiminlu@zju.edu.cn.ORCID http://orcid.org/0000-0002-2859-2736
Daqian XuZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China. xudaqian@zju.edu.cn.ORCID http://orcid.org/0000-0003-0478-2997
Zhejiang University · CNZhejiang Cancer Hospital · CNHarbin Medical University · CNQingdao University · CNThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of receptor protein kinases is prevalent in various cancers with unknown impact on ferroptosis. Here we demonstrated that AKT activated by insulin-like growth factor 1 receptor signalling phosphorylates creatine kinase B (CKB) T133, reduces metabolic activity of CKB and increases CKB binding to glutathione peroxidase 4 (GPX4). Importantly, CKB acts as a protein kinase and phosphorylates GPX4 S104. This phosphorylation prevents HSC70 binding to GPX4, thereby abrogating the GPX4 degradation regulated by chaperone-mediated autophagy, alleviating ferroptosis and promoting tumour growth in mice. In addition, the levels of GPX4 are positively correlated with the phosphorylation levels of CKB T133 and GPX4 S104 in human hepatocellular carcinoma specimens and associated with poor prognosis of patients with hepatocellular carcinoma. These findings reveal a critical mechanism by which tumour cells counteract ferroptosis by non-metabolic function of CKB-enhanced GPX4 stability and underscore the potential to target the protein kinase activity of CKB for cancer treatment.

Indexed as

Carcinoma, HepatocellularFerroptosisLiver NeoplasmsAnimalsCreatine KinaseHumansMicePhospholipid Hydroperoxide Glutathione PeroxidasePhosphorylationCreatine Kinaseglutathione peroxidase 4, mouseGPX4 protein, humanPhospholipid Hydroperoxide Glutathione Peroxidase

Identifiers

PMID37156912
OpenAlexW4375861575

What OpenQuestion holds

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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.