Evidence map›Paper›PMID 38654109›Full record

ArticleOncogene2024

P4HA2 activates mTOR via hydroxylation and targeting P4HA2-mTOR inhibits lung adenocarcinoma cell growth.

Ersuo Jin, Shengjie Wang, Donglai Chen, Jia-Ping Wang, Yuanyuan Zeng, Runfeng Sun, Hong-Tao Zhang

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  4. Targeting collagen Prolyl 4-hydroxylase for cancer treatment.Medical oncology (Northwood, London, England) · 2025
    Review
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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

7 authors at 2 institutions in 1 country.

Ersuo Jin *Soochow University Laboratory of Cancer Molecular Genetics, Collaborative Innovation Center of Molecular Medicine between Soochow University and Donghai County People's Hospital, Suzhou Medical College of Soochow University, Suzhou, 215123, Jiangsu Province, China.
Shengjie Wang *Soochow University Laboratory of Cancer Molecular Genetics, Collaborative Innovation Center of Molecular Medicine between Soochow University and Donghai County People's Hospital, Suzhou Medical College of Soochow University, Suzhou, 215123, Jiangsu Province, China.ORCID 0000-0003-0320-0377
Donglai Chen *Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.ORCID 0000-0001-7603-4803
Jia-Ping WangSoochow University Laboratory of Cancer Molecular Genetics, Collaborative Innovation Center of Molecular Medicine between Soochow University and Donghai County People's Hospital, Suzhou Medical College of Soochow University, Suzhou, 215123, Jiangsu Province, China.
Yuanyuan ZengDepartment of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou Medical College of Soochow University, Suzhou, 215006, Jiangsu Province, China.
Runfeng SunSoochow University Laboratory of Cancer Molecular Genetics, Collaborative Innovation Center of Molecular Medicine between Soochow University and Donghai County People's Hospital, Suzhou Medical College of Soochow University, Suzhou, 215123, Jiangsu Province, China. 13851211100@139.com.ORCID 0009-0009-7908-0106
Hong-Tao ZhangSoochow University Laboratory of Cancer Molecular Genetics, Collaborative Innovation Center of Molecular Medicine between Soochow University and Donghai County People's Hospital, Suzhou Medical College of Soochow University, Suzhou, 215123, Jiangsu Province, China. htzhang@suda.edu.cn.ORCID 0000-0003-4182-421X
Soochow University · CNFudan University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82273372
6 · The paper itself

Abstract

Mammalian target of rapamycin (mTOR) kinase functions as a central regulator of cell growth and metabolism, and its complexes mTORC1 and mTORC2 phosphorylate distinct substrates. Dysregulation of mTOR signaling is commonly implicated in human diseases, including cancer. Despite three decades of active research in mTOR, much remains to be determined. Here, we demonstrate that prolyl 4-hydroxylase alpha-2 (P4HA2) binds directly to mTOR and hydroxylates one highly conserved proline 2341 (P2341) within a kinase domain of mTOR, thereby activating mTOR kinase and downstream effector proteins (e.g. S6K and AKT). Moreover, the hydroxylation of P2341 strengthens mTOR stability and allows mTOR to accurately recognize its substrates such as S6K and AKT. The growth of lung adenocarcinoma cells overexpressing mTOR

Indexed as

Adenocarcinoma of LungCell ProliferationLung NeoplasmsTOR Serine-Threonine KinasesAnimalsCell Line, TumorHumansHydroxylationMiceProcollagen-Proline DioxygenaseSignal TransductionMTOR protein, humanProcollagen-Proline DioxygenaseTOR Serine-Threonine Kinases

Identifiers

PMID38654109
PMCPMC11164680
OpenAlexW4395037778

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.