Evidence map›Paper›PMID 35177822›Full record

ArticleNature cell biology2022

YAP/TAZ drives cell proliferation and tumour growth via a polyamine-eIF5A hypusination-LSD1 axis.

Hongde Li, Bo-Kuan Wu, Mohammed Kanchwala, Jing Cai, Li Wang, Chao Xing, Yonggang Zheng, Duojia Pan

Open access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
7.7field-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

72 citing papers in PubMed, 93 citations in OpenAlex.

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12 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 2 institutions in 1 country.

Hongde LiDepartment of Physiology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID http://orcid.org/0000-0003-1256-2513
Bo-Kuan WuDepartment of Physiology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Mohammed KanchwalaEugene McDermott Center for Human Growth and Development/Center for Human Genetics, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID http://orcid.org/0000-0001-6035-2970
Jing CaiDepartment of Physiology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Li WangDepartment of Physiology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Chao XingEugene McDermott Center for Human Growth and Development/Center for Human Genetics, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID http://orcid.org/0000-0002-1838-0502
Yonggang ZhengDepartment of Physiology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID http://orcid.org/0000-0002-3326-4614
Duojia PanDepartment of Physiology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. duojia.pan@utsouthwestern.edu.ORCID http://orcid.org/0000-0003-2890-4645
Howard Hughes Medical Institute · USCenter for Human Genetics · US

Funding

Control of Cell Number in Developing RetinaR01EY015708 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI DUOJIA PAN · 2004 to 2026
$8.8M
Howard Hughes Medical InstituteNEI NIH HHS R01 EY015708
6 · The paper itself

Abstract

Metabolic reprogramming is central to oncogene-induced tumorigenesis by providing the necessary building blocks and energy sources, but how oncogenic signalling controls metabolites that play regulatory roles in driving cell proliferation and tumour growth is less understood. Here we show that oncogene YAP/TAZ promotes polyamine biosynthesis by activating the transcription of the rate-limiting enzyme ornithine decarboxylase 1. The increased polyamine levels, in turn, promote the hypusination of eukaryotic translation factor 5A (eIF5A) to support efficient translation of histone demethylase LSD1, a transcriptional repressor that mediates a bulk of YAP/TAZ-downregulated genes including tumour suppressors in YAP/TAZ-activated cells. Accentuating the importance of the YAP/TAZ-polyamine-eIF5A hypusination-LSD1 axis, inhibiting polyamine biosynthesis or LSD1 suppressed YAP/TAZ-induced cell proliferation and tumour growth. Given the frequent upregulation of YAP/TAZ activity and polyamine levels in diverse cancers, our identification of YAP/TAZ as an upstream regulator and LSD1 as a downstream effector of the oncometabolite polyamine offers a molecular framework in which oncogene-induced metabolic and epigenetic reprogramming coordinately drives tumorigenesis, and suggests potential therapeutic strategies in YAP/TAZ- or polyamine-dependent human malignancies.

Indexed as

Adaptor Proteins, Signal TransducingNeoplasmsCarcinogenesisCell ProliferationHistone DemethylasesHumansPhosphoproteinsPolyaminesTrans-ActivatorsYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingHistone DemethylasesPhosphoproteinsPolyaminesTrans-ActivatorsYAP-Signaling Proteins

Identifiers

PMID35177822
PMCPMC8930503
OpenAlexW4213001467

What OpenQuestion holds

Textmetadata
LicenceTDM
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.