Evidence map›Paper›PMID 30397197›Full record

ArticleNature communications2018

Inhibition of mTORC1 by lncRNA H19 via disrupting 4E-BP1/Raptor interaction in pituitary tumours.

Ze Rui Wu, Lichong Yan, Yan Ting Liu, Lei Cao, Yu Hang Guo, Yong Zhang, Hong Yao, Lin Cai, Han Bing Shang, Wei Wei Rui and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
7.0field-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

76 citing papers in PubMed, 140 citations in OpenAlex.

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  9. Long noncoding RNAs in ubiquitination, protein degradation, and human diseases.Biochimica et biophysica acta. Gene regulatory mechanisms · 2024
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16 more citing papers are in PubMed but not listed here.

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

19 authors at 5 institutions in 2 countries.

Ze Rui WuDepartment of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.
Lichong YanShanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.
Yan Ting LiuDepartment of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.
Lei CaoDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, 100050, Beijing, China.
Yu Hang GuoDepartment of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University, 325000, Wenzhou, China.
Yong ZhangDepartment of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.
Hong YaoDepartment of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.
Lin CaiDepartment of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University, 325000, Wenzhou, China.
Han Bing ShangDepartment of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.
Wei Wei RuiDepartment of Pathology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.
Gang YangDepartment of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, 410000, Chongqing, China.
Xiao Biao ZhangDepartment of Neurosurgery, Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Hao TangDepartment of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.
Yu WangDepartment of Neurosurgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 200127, Shanghai, China.
Jin Yan HuangState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.ORCID http://orcid.org/0000-0002-8053-0209
Yong Xu WeiDepartment of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.
Wei Guo ZhaoDepartment of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.
Bing SuShanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. bingsu@sjtu.edu.cn.
Zhe Bao WuDepartment of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. zhebaowu@aliyun.com.ORCID http://orcid.org/0000-0002-1611-8228
Shanghai Jiao Tong University · CNWenzhou Medical University · CNCapital Medical University · CNSun Yat-sen University · CNThe Affiliated Yongchuan Hospital of Chongqing Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31470845National Natural Science Foundation of China (National Science Foundation of China) 81271523National Natural Science Foundation of China (National Science Foundation of China) 81430033National Natural Science Foundation of China (National Science Foundation of China) 81671371
6 · The paper itself

Abstract

Aberrant expression of long noncoding RNA H19 has been associated with tumour progression, but the underlying molecular tumourigenesis mechanisms remain largely unknown. Here, we report that H19 expression is frequently downregulated in human primary pituitary adenomas and is negatively correlated with tumour progression. Consistently, upregulation of H19 expression inhibits pituitary tumour cell proliferation in vitro and tumour growth in vivo. Importantly, we uncover a function of H19, which controls cell/tumour growth through inhibiting function of mTORC1 but not mTORC2. Mechanistically, we show that H19 could block mTORC1-mediated 4E-BP1 phosphorylation without affecting S6K1 activation. At the molecular level, H19 interacted with 4E-BP1 at the TOS motif and competitively inhibited 4E-BP1 binding to Raptor. Finally, we demonstrate that H19 is more effective than cabergoline treatment in the suppression of pituitary tumours. Together, our study uncovered the role of H19-mTOR-4E-BP1 axis in pituitary tumour growth regulation that may be a potential therapeutic target for human pituitary tumours.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCabergolineCarcinogenesisCarrier ProteinsCell Cycle ProteinsCell Line, TumorCell ProliferationDisease ProgressionDown-RegulationFemaleHEK293 CellsHeterograftsHumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Adaptor Proteins, Signal TransducingCabergolineCarrier ProteinsCell Cycle ProteinsEIF4EBP1 protein, humanH19 long non-coding RNAMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Phosphoproteinsribosomal protein S6 kinase, 70kD, polypeptide 1Ribosomal Protein S6 Kinases, 70-kDaRNA, Long Noncoding

Identifiers

PMID30397197
PMCPMC6218470
OpenAlexW2899178572

What OpenQuestion holds

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LicenceCC BY
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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.