Evidence map›Paper›PMID 30531839›Full record

ArticleOncogene2019

Cell type-dependent function of LATS1/2 in cancer cell growth.

Wei-Wei Pan, Toshiro Moroishi, Ja Hyun Koo, Kun-Liang Guan

Abstract read
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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Review
  8. Proximal TubularInternational journal of molecular sciences · 2023
    Article
  9. Article
  10. New insights into the ambivalent role of YAP/TAZ in human cancers.Journal of experimental & clinical cancer research : CR · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Non-canonical role of Hippo tumor suppressor serine/threonine kinase 3 STK3 in prostate cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  17. Article
  18. Article
  19. Review
  20. Article
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

4 authors at 2 institutions in 3 countries.

Wei-Wei PanDepartment of Pharmacology and Moores Cancer Center, University of California, San Diego, La Jolla, CA, 92093, USA. aidspan@163.com.
Toshiro MoroishiDepartment of Pharmacology and Moores Cancer Center, University of California, San Diego, La Jolla, CA, 92093, USA.ORCID http://orcid.org/0000-0001-6419-3882
Ja Hyun KooDepartment of Pharmacology and Moores Cancer Center, University of California, San Diego, La Jolla, CA, 92093, USA.
Kun-Liang GuanDepartment of Pharmacology and Moores Cancer Center, University of California, San Diego, La Jolla, CA, 92093, USA. kuguan@ucsd.edu.ORCID http://orcid.org/0000-0003-1892-0174
University of California San Diego · USKumamoto Health Science University · JP

Funding

PROTEIN PHOSPHORYLATION AND GROWTH FACTOR FUNCTIONR01GM051586 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROWN, JOAN HELLER · 1994 to 2024
$7.9M
The mTOR and Hippo pathway in cell growth and cancerR35CA196878 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUAN, KUN-LIANG · 2015 to 2019
$4.0M
Molecular Mechanism and Therapy for Ocular MelanomaR01CA217642 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER · 2017 to 2022
$2.4M
Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) CA196878NCI NIH HHS R01 CA217642NCI NIH HHS R35 CA196878NIGMS NIH HHS R01 GM051586
6 · The paper itself

Abstract

The Hippo pathway controls organ size and tissue homeostasis, and its dysregulation often contributes to tumorigenesis. Extensive studies have shown that the Hippo pathway inhibits cell proliferation, and survival in a cell-autonomous manner. We examined the function of the Hippo pathway kinases LATS1/2 (large tumor suppressor 1 and 2) in cancer cells. As expected, loss of LATS1/2 promotes cancer cell growth in most cell lines. Surprisingly, however, LATS1/2 deletion inhibits the growth of murine MC38 colon cancer cells, especially under detachment conditions. This growth inhibitory effect caused by LATS1/2 deletion is due to uncontrolled activation of Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), the key downstream transcriptional coactivators inhibited by LATS1/2. We identified Wnt inducible signaling pathway protein 2 (Wisp2) and coiled-coil domain containing 80 (Ccdc80) as direct targets of YAP/TAZ. Their expression is selectively induced by LATS1/2 deletion in MC38 cells. Furthermore, deletion of WISP2 and CCDC80 prevents the growth inhibitory effect of LATS1/2 loss in MC38 cells. Our study demonstrates that the function of LATS1/2 in cell growth is cell context dependent, suggesting that LATS1/2 inhibition can be a therapeutic approach for some cancer types.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCarcinogenesisCell LineCell Line, TumorCell ProliferationFemaleHEK293 CellsHumansIntercellular Signaling Peptides and ProteinsMiceMice, NudeProtein Serine-Threonine KinasesRepressor ProteinsSignal TransductionTranscriptional ActivationAdaptor Proteins, Signal TransducingIntercellular Signaling Peptides and ProteinsLats1 protein, mouseLATS2 protein, mouseProtein Serine-Threonine KinasesRepressor ProteinsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID30531839
PMCPMC6450751
OpenAlexW2904975871

What OpenQuestion holds

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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.