Evidence map›Paper›PMID 31853539›Full record

ArticleNucleic acids research2020

Integrative analyses of noncoding RNAs reveal the potential mechanisms augmenting tumor malignancy in lung adenocarcinoma.

Jou-Ho Shih, Hsin-Yi Chen, Shin-Chih Lin, Yi-Chen Yeh, Roger Shen, Yaw-Dong Lang, Dung-Chi Wu, Chien-Yu Chen, Ruey-Hwa Chen, Teh-Ying Chou and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

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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

11 authors at 6 institutions in 1 country.

Jou-Ho ShihGenome and Systems Biology Program, National Taiwan University and Academia Sinica, Taipei 10617, Taiwan.
Hsin-Yi ChenGraduate Institute of Cancer Biology & Drug Discovery, College of Medical Science & Technology, Taipei Medical University, Taipei 11221, Taiwan.
Shin-Chih LinProgram in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11221, Taiwan.
Yi-Chen YehDivision of Molecular Pathology, Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei 11221, Taiwan.
Roger ShenInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Yaw-Dong LangInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Dung-Chi WuGenome and Systems Biology Program, National Taiwan University and Academia Sinica, Taipei 10617, Taiwan.
Chien-Yu ChenGenome and Systems Biology Program, National Taiwan University and Academia Sinica, Taipei 10617, Taiwan.
Ruey-Hwa ChenInstitute of Biological Chemistry, Academia Sinica, Taipei 11529, Taiwan.
Teh-Ying ChouProgram in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11221, Taiwan.
Yuh-Shan JouGenome and Systems Biology Program, National Taiwan University and Academia Sinica, Taipei 10617, Taiwan.
National Yang Ming Chiao Tung University · TWNational Taiwan University · TWInstitute of Biological Chemistry, Academia Sinica · TWInstitute of Biomedical Sciences, Academia Sinica · TWTaipei Medical University · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Precise noncoding RNA (ncRNA)-based network prediction is necessary to reveal ncRNA functions and pathological mechanisms. Here, we established a systemic pipeline to identify prognostic ncRNAs, predict their functions and explore their pathological mechanisms in lung adenocarcinoma (LUAD). After in silico and experimental validation based on evaluations of prognostic value in multiple LUAD cohorts, we selected the PTTG3P pseudogene from among other prognostic ncRNAs (MIR497HG, HSP078, TBX5-AS1, LOC100506990 and C14orf64) for mechanistic studies. PTTG3P upregulation in LUAD cells shortens the metaphase to anaphase transition in mitosis, increases cell viability after cisplatin or paclitaxel treatment, facilitates tumor growth that leads to poor survival in orthotopic lung models, and is associated with a poor survival rate in LUAD patients in the TCGA cohort who received chemotherapy. Mechanistically, PTTG3P acts as an ncRNA that interacts with the transcription factor FOXM1 to regulate the transcriptional activation of the mitotic checkpoint kinase BUB1B, which augments tumor growth and chemoresistance and leads to poor outcomes for LUAD patients. Overall, we established a systematic strategy to uncover prognostic ncRNAs with functional prediction methods suitable for pan-cancer studies. Moreover, we revealed that PTTG3P, due to its upregulation of the PTTG3P/FOXM1/BUB1B axis, could be a therapeutic target for LUAD patients.

Indexed as

AdenocarcinomaAnimalsCell Cycle ProteinsCell Line, TumorCell ProliferationChromatinComputer SimulationDrug Resistance, NeoplasmForkhead Box Protein M1HumansLung NeoplasmsMaleMiceMitosisPrognosisProtein Serine-Threonine KinasesBUB1B protein, humanCell Cycle ProteinsChromatinForkhead Box Protein M1Protein Serine-Threonine KinasesRNA, Untranslated

Identifiers

PMID31853539
PMCPMC7026595
OpenAlexW2994871979

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.