Evidence map›Paper›PMID 30967631›Full record

ArticleOncogene2019

LncRNA NORAD is repressed by the YAP pathway and suppresses lung and breast cancer metastasis by sequestering S100P.

Boon-Shing Tan, Min-Chi Yang, Shaifali Singh, Yu-Chi Chou, Hsin-Yi Chen, Ming-Yang Wang, Yi-Ching Wang, Ruey-Hwa Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
10.6field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

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  18. Cancers · 2024
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  19. Fibroblasts: invigorated targets in pre-metastatic niche formation.International journal of biological sciences · 2024
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21 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

8 authors at 8 institutions in 1 country.

Boon-Shing TanInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Min-Chi YangInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Shaifali SinghInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Yu-Chi ChouGenomic Research Center, Academia Sinica, Taipei, Taiwan.
Hsin-Yi ChenGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Ming-Yang WangDepartment of Surgery, National Taiwan University Hospital, Taipei, Taiwan.
Yi-Ching WangInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Ruey-Hwa ChenInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan. rhchen@gate.sinica.edu.tw.
Academia Sinica · TWGenomics Research Center, Academia Sinica · TWInstitute of Biological Chemistry, Academia Sinica · TWNational Cheng Kung University · TWNational Taiwan University · TWNational Taiwan University Hospital · TWNational Tsing Hua University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is responsible for most cancer mortality, but its molecular mechanism has not been completely understood. In addition to coding genes and miRNAs, the contribution of long noncoding RNAs (lncRNAs) to tumor metastatic dissemination and the mechanisms controlling their expression are areas of intensive investigation. Here, we show that lncRNA NORAD is downregulated in lung and breast cancers, and that NORAD low expression in these cancer types is associated with lymph node metastasis and poor prognosis. NORAD is transcriptionally repressed by the Hippo pathway transducer YAP/TAZ-TEAD complex in conjunction with the action of NuRD complex. Functionally, NORAD elicits potent inhibitory effects on migration and invasion of multiple lung and breast cancer cell lines, and repression of NORAD expression participates in the migration- and invasion-stimulatory effects of the YAP pathway. Mechanistically, NORAD exploits its multiple repeated sequences to function as a multivalent platform for binding and sequestering S100P, thereby suppressing S100P-elicited pro-metastatic signaling network. Using cell and mouse models, we show that the S100P decoy function of NORAD suppresses lung and breast cancer migration, invasion, and metastasis. Together, our study identifies NORAD as a novel metastasis suppressor, elucidates its regulatory and functional mechanisms, and highlights its prognostic value.

Indexed as

Neoplasm MetastasisAdaptor Proteins, Signal TransducingBreast NeoplasmsCalcium-Binding ProteinsCell Line, TumorDown-RegulationFemaleHumansLung NeoplasmsMass SpectrometryNeoplasm InvasivenessNeoplasm ProteinsPrognosisProtein BindingRNA, Long NoncodingTranscription FactorsAdaptor Proteins, Signal TransducingCalcium-Binding ProteinsNeoplasm ProteinsNORAD long non-coding RNA, humanRNA, Long NoncodingS100P protein, humanTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID30967631
OpenAlexW2936557674

What OpenQuestion holds

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Read underepoch 390

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.