Evidence map›Paper›PMID 31848340›Full record

ArticleNature communications2019

LATS1 but not LATS2 represses autophagy by a kinase-independent scaffold function.

Fengyuan Tang, Ruize Gao, Beena Jeevan-Raj, Christof B Wyss, Ravi K R Kalathur, Salvatore Piscuoglio, Charlotte K Y Ng, Sravanth K Hindupur, Sandro Nuciforo, Eva Dazert and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 68 citations in OpenAlex.

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  7. Clear cell renal carcinoma essentially requires CDKL3 for oncogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

21 authors at 5 institutions in 3 countries.

Fengyuan TangDepartment of Biomedicine, University of Basel, Basel, Switzerland. fengyuan.tang@unibas.ch.
Ruize GaoDepartment of Biomedicine, University of Basel, Basel, Switzerland.
Beena Jeevan-RajDepartment of Biomedicine, University of Basel, Basel, Switzerland.
Christof B WyssDepartment of Biomedicine, University of Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0001-7248-0574
Ravi K R KalathurDepartment of Biomedicine, University of Basel, Basel, Switzerland.
Salvatore PiscuoglioInstitute of Pathology, University Hospital Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0003-2686-2939
Charlotte K Y NgInstitute of Pathology, University Hospital Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0002-6100-0026
Sravanth K HindupurBiozentrum, University of Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0002-8078-4006
Sandro NuciforoDepartment of Biomedicine, University of Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0002-1863-1869
Eva DazertBiozentrum, University of Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0002-7292-2261
Thomas BockBiozentrum, University of Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0002-9314-5318
Shuang SongFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
David BuechelDepartment of Biomedicine, University of Basel, Basel, Switzerland.
Marco F MoriniDepartment of Biomedicine, University of Basel, Basel, Switzerland.
Alexander HergovichUCL Cancer Institute, University College London, London, WC1E 6BT, UK.
Patrick MatthiasFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.ORCID http://orcid.org/0000-0002-3927-1452
Dae-Sik LimKorea Advanced Institute of Science and Technology, Daejeon, 34141, Republic of Korea.
Luigi M TerraccianoInstitute of Pathology, University Hospital Basel, Basel, Switzerland.
Markus H HeimDepartment of Biomedicine, University of Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0002-7523-4894
Michael N HallBiozentrum, University of Basel, Basel, Switzerland.
Gerhard ChristoforiDepartment of Biomedicine, University of Basel, Basel, Switzerland. gerhard.christofori@unibas.ch.
University of Basel · CHUniversity Hospital of Basel · CHFriedrich Miescher Institute · CHKorea Advanced Institute of Science and Technology · KRUniversity College London · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Autophagy perturbation represents an emerging therapeutic strategy in cancer. Although LATS1 and LATS2 kinases, core components of the mammalian Hippo pathway, have been shown to exert tumor suppressive activities, here we report a pro-survival role of LATS1 but not LATS2 in hepatocellular carcinoma (HCC) cells. Specifically, LATS1 restricts lethal autophagy in HCC cells induced by sorafenib, the standard of care for advanced HCC patients. Notably, autophagy regulation by LATS1 is independent of its kinase activity. Instead, LATS1 stabilizes the autophagy core-machinery component Beclin-1 by promoting K27-linked ubiquitination at lysine residues K32 and K263 on Beclin-1. Consequently, ubiquitination of Beclin-1 negatively regulates autophagy by promoting inactive dimer formation of Beclin-1. Our study highlights a functional diversity between LATS1 and LATS2, and uncovers a scaffolding role of LATS1 in mediating a cross-talk between the Hippo signaling pathway and autophagy.

Indexed as

AnimalsAutophagyBeclin-1Carcinoma, HepatocellularCell Line, TumorCell ProliferationCell SurvivalDatasets as TopicDisease-Free SurvivalDrug Resistance, NeoplasmHippo Signaling PathwayHumansKaplan-Meier EstimateLiverLiver NeoplasmsLysineBeclin-1BECN1 protein, humanLATS1 protein, humanLats1 protein, mouseLATS2 protein, humanLysineProtein Serine-Threonine KinasesSorafenibTumor Suppressor Proteins

Identifiers

PMID31848340
PMCPMC6917744
OpenAlexW2995282383

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.