Evidence map›Paper›PMID 39815301›Full record

ArticleMolecular cancer2025

ALKBH5 suppresses gastric cancer tumorigenesis and metastasis by inhibiting the translation of uncapped WRAP53 RNA isoforms in an m6A-dependent manner.

Ziqi Zheng, Feizhi Lin, Baiwei Zhao, Guoming Chen, Chengzhi Wei, Xiaojiang Chen, Runcong Nie, Ruopeng Zhang, Zhoukai Zhao, Zhiwei Zhou and 4 more

Abstract read
In one paragraph

Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Article
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  3. The Role of NMedComm · 2026
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  5. RNA mCell biology and toxicology · 2026
    Review
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  13. Targeting of the mNature communications · 2025
    Article
  14. Review
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  16. Article
  17. The mMolecular biomedicine · 2025
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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.

Ziqi Zheng *Department of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
Feizhi Lin *Department of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
Baiwei Zhao *Department of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
Guoming Chen *Department of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
Chengzhi WeiDepartment of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
Xiaojiang ChenDepartment of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
Runcong NieDepartment of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
Ruopeng ZhangDepartment of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
Zhoukai ZhaoDepartment of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
Zhiwei ZhouDepartment of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China.
Yuanfang LiDepartment of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China. liyuanf@sysucc.org.cn.
Weigang DaiCenter of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-Sen University, No.58 Zhongshan Er Road, Guangzhou, 510060, P. R. China. daiweig@mail.sysu.edu.cn.
Yijia LinDepartment of General Surgery (Gastrointestinal Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, NO. 26 Yuancun Erheng Road, Guangzhou, 510060, People's Republic of China. linyj3@mail.sysu.edu.cn.
Yongming ChenDepartment of Gastric Surgery, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, No. 651 Dongfeng Road East, Guangzhou, 510060, People's Republic of China. chenyongm@sysucc.org.cn.

Funding

China Postdoctoral Science Foundation 2022TQ0390National Natural Science Foundation of China 82103586National Natural Science Foundation of China 82303803
6 · The paper itself

Abstract

The N6-methyladenosine (m6A) modification serves as an essential epigenetic regulator in eukaryotic cells, playing a significant role in tumorigenesis and cancer progression. However, the detailed biological functions and underlying mechanisms of m6A regulation in gastric cancer (GC) are poorly understood. Our research revealed that the m6A demethylase ALKBH5 was markedly downregulated in GC tissues, which was associated with poor patient prognosis. Functional studies demonstrated that suppressing ALKBH5 expression enhanced GC cell proliferation, migration, and invasion. Mechanistically, ALKBH5 removed m6A modifications from the 5' uncapped and polyadenylated transcripts (UPTs) of WRAP53. This demethylation decreased WRAP53 stability and translation efficiency. The lower level of WRAP53 disrupts the interaction between USP6 and RALBP1 protein, promoting RALBP1 degradation and thereby suppressing the PI3K/Akt/mTOR signaling cascade, ultimately attenuating the progression of GC. These findings highlight the pivotal role of ALKBH5-mediated m6A demethylation in inhibiting GC progression and the potential role of ALKBH5 as a promising biomarker and therapeutic target for GC intervention.

Indexed as

AdenosineAlkB Homolog 5, RNA DemethylaseStomach NeoplasmsAnimalsCarcinogenesisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMiceNeoplasm MetastasisPrognosisProtein BiosynthesisSignal TransductionAdenosineALKBH5 protein, humanAlkB Homolog 5, RNA DemethylaseN-methyladenosineALKBH5Gastric cancerM6AMetastasisWRAP53

Identifiers

PMID39815301
PMCPMC11734446

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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.