Evidence map›Paper›PMID 34845189›Full record

ArticleCell death discovery2021

LncRNA SFTA1P mediates positive feedback regulation of the Hippo-YAP/TAZ signaling pathway in non-small cell lung cancer.

Bowen Zhu, Megan Finch-Edmondson, Kim Whye Leong, Xiaoqian Zhang, Mitheera V, Quy Xiao Xuan Lin, Yaelim Lee, Wei Ting Ng, Huili Guo, Yue Wan and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 22 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

12 authors at 2 institutions in 2 countries.

Bowen ZhuGenome Institute of Singapore (GIS), Agency for Science, Technology and Research (A*STAR), Singapore, 138672, Singapore.
Megan Finch-EdmondsonMechanobiology Institute (MBI), National University of Singapore, Singapore, 117411, Singapore.
Kim Whye LeongGenome Institute of Singapore (GIS), Agency for Science, Technology and Research (A*STAR), Singapore, 138672, Singapore.
Xiaoqian ZhangGenome Institute of Singapore (GIS), Agency for Science, Technology and Research (A*STAR), Singapore, 138672, Singapore.
Mitheera VGenome Institute of Singapore (GIS), Agency for Science, Technology and Research (A*STAR), Singapore, 138672, Singapore.
Quy Xiao Xuan LinCancer Science Institute of Singapore, National University of Singapore, Singapore, 117599, Singapore.ORCID http://orcid.org/0000-0002-7167-2627
Yaelim LeeMechanobiology Institute (MBI), National University of Singapore, Singapore, 117411, Singapore.
Wei Ting NgInstitute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), Singapore, 138673, Singapore.
Huili GuoInstitute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), Singapore, 138673, Singapore.
Yue WanGenome Institute of Singapore (GIS), Agency for Science, Technology and Research (A*STAR), Singapore, 138672, Singapore.
Marius SudolDepartment of Physiology, NUS Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117593, Singapore.
Ramanuj DasGuptaGenome Institute of Singapore (GIS), Agency for Science, Technology and Research (A*STAR), Singapore, 138672, Singapore. dasguptar@gis.a-star.edu.sg.ORCID http://orcid.org/0000-0001-9015-3729
Agency for Science, Technology and Research · SGNational University of Singapore · SG

Funding

Agency for Science, Technology and Research (A*STAR) CoreMechanobiology Institute, Singapore (Mechanobiology Institute) R-714-018-0060271MOH | National Medical Research Council (NMRC) NMRC/OFIRG/0044/2017National University of Singapore (NUS) NUS Research scholarshipNational University of Singapore (NUS) R-185-000-2710-133;733
6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) regulate numerous biological processes involved in both development and carcinogenesis. Hippo-YAP/TAZ signaling, a critical pathway responsible for organ size control, is often dysregulated in a variety of cancers. However, the nature and function of YAP/TAZ-regulated lncRNAs during tumorigenesis remain largely unexplored. By profiling YAP/TAZ-regulated lncRNAs, we identified SFTA1P as a novel transcriptional target and a positive feedback regulator of YAP/TAZ signaling. Using non-small cell lung cancer (NSCLC) cell lines, we show that SFTA1P is transcriptionally activated by YAP/TAZ in a TEAD-dependent manner. Functionally, knockdown of SFTA1P in NSCLC cell lines inhibited proliferation, induced programmed cell death, and compromised their tumorigenic potential. Mechanistically, SFTA1P knockdown decreased TAZ protein abundance and consequently, the expression of YAP/TAZ transcriptional targets. We provide evidence that this phenomenon could potentially be mediated via its interaction with TAZ mRNA to regulate TAZ translation. Our results reveal SFTA1P as a positive feedback regulator of Hippo-YAP/TAZ signaling, which may serve as the molecular basis for lncRNA-based therapies against YAP/TAZ-driven cancers.

Identifiers

PMID34845189
PMCPMC8630011
OpenAlexW3216687547

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.