Evidence map›Paper›PMID 39438763›Full record

ArticleOncogene2025

Zinc ions activate AKT and promote prostate cancer cell proliferation via disrupting AKT intramolecular interaction.

Kangjunjie Wang, Min Chen, Shukun Yan, Ying Han, Huairui Yuan, Qiuli Liu, Dayun Lu, Long Li, Kaihua Wang, Fen Liu and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

17 authors.

Kangjunjie Wang *Key Laboratory of Systems Health Science of Zhejiang Province, School of Life Science, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, 310024, China.ORCID 0000-0002-9580-5041
Min Chen *Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, 201203, Shanghai, China.
Shukun Yan *University of Chinese Academy of Sciences, Number 19A Yuquan Road, Beijing, 100049, China.
Ying HanCAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai, 200031, China.
Huairui YuanKey Laboratory of Multi-Cell Systems, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, 200031, China.
Qiuli LiuDepartment of Urology, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing, 400042, China.ORCID 0000-0002-9532-5654
Dayun LuDepartment of Analytical Chemistry and CAS Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai, 201203, China.
Long LiKey Laboratory of Multi-Cell Systems, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, 200031, China.
Kaihua WangKey Laboratory of Multi-Cell Systems, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, 200031, China.
Fen LiuKey Laboratory of Multi-Cell Systems, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, 200031, China.
Qianqian LiKey Laboratory of Multi-Cell Systems, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, 200031, China.
Dakui LuoDepartment of Colorectal Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Jun JiangDepartment of Urology, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing, 400042, China.ORCID 0000-0001-9408-2972
Hu ZhouUniversity of Chinese Academy of Sciences, Number 19A Yuquan Road, Beijing, 100049, China.ORCID 0000-0001-7006-4737
Yong ChenKey Laboratory of Systems Health Science of Zhejiang Province, School of Life Science, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, 310024, China. yongchen@sibcb.ac.cn.ORCID 0000-0001-5857-6086
Jun QinUniversity of Chinese Academy of Sciences, Number 19A Yuquan Road, Beijing, 100049, China. qinjun@sibs.ac.cn.ORCID 0000-0002-2263-128X
Daming GaoKey Laboratory of Systems Health Science of Zhejiang Province, School of Life Science, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, 310024, China. dgao@sibcb.ac.cn.ORCID 0000-0003-4374-1055

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32221002National Natural Science Foundation of China (National Science Foundation of China) 81790253National Natural Science Foundation of China (National Science Foundation of China) 81925029National Natural Science Foundation of China (National Science Foundation of China) 82230098
6 · The paper itself

Abstract

Prostate is a zinc rich organ and the physiological function of the abundant zinc ions is relatively less understood. AKT kinase is a pivotal regulator downstream of cytokines, growth factors and other extracellular stimuli, and the attachment of its PH domain to PtdIns-3,4,5-P3 (PIP3) and the subsequent phosphorylation of its kinase domain by PDPK1 are considered important for its activation. Herein, we report a regulatory mechanism of AKT kinase by zinc ions. Mechanistically, zinc ions directly bind to AKT and facilitate AKT activation through disrupting the interaction between PH and kinase domains within AKT molecule. Consistently, AKT1-H89A/E91A mutant (zinc-binding-deficient) fails to respond to zinc ions and exhibits strong interaction between PH and kinase domains, and it is less oncogenic in orthotopic xenograft model of prostate cancer. On the other hand, the AKT1-W80L mutant with minimum intra-molecular interaction between PH and kinase domains shows strong tumor promoting capacity although it could not be further stimulated by zinc ions. Overall, this study reveals a distinctive regulatory mechanism of AKT activation and implies a tumor promoting role of the zinc ions in prostate cancer.

Indexed as

Cell ProliferationProstatic NeoplasmsProto-Oncogene Proteins c-aktZincAnimalsCell Line, TumorEnzyme ActivationHumansMaleMicePhosphorylationAKT1 protein, humanProto-Oncogene Proteins c-aktZinc

Identifiers

PMID39438763

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.