Evidence map›Paper›PMID 21278236›Full record

ArticleCancer research2011

Identification of a tumor suppressor relay between the FOXP3 and the Hippo pathways in breast and prostate cancers.

Weiquan Li, Lizhong Wang, Hiroto Katoh, Runhua Liu, Pan Zheng, Yang Liu

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 7% 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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.

  1. The association ofBioscience reports · 2019
    Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Disease markers · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. FOXP3 expression in FOXP3Translational cancer research · 2020
    Article
  14. Article
  15. Review
  16. Article
  17. FOXP3 Activates SUMO-ConjugatingInternational journal of molecular sciences · 2018
    Article
  18. Article
  19. Article
  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

6 authors at 1 institution in 1 country.

Weiquan LiDepartments of Surgery, Pathology, and Internal Medicine, Division of Immunotherapy, University of Michigan School of Medicine and Cancer Center, Ann Arbor, Michigan 48109, USA.
Lizhong Wang
Hiroto Katoh
Runhua Liu
Pan Zheng
Yang Liu
University of Michigan–Ann Arbor · US

Funding

Tumor burden and T cell immunityR01CA058033 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIU, YANG · 1992 to 2013
$3.3M
mTOR, Inflammation and Senescence of Hematopoietic Stem CellsR01AG036690 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ZHENG, PAN · 2010 to 2014
$1.6M
FoxP3 as the X-Linked Breast Cancer Suppressor GeneR01CA120901 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIU, YANG · 2007 to 2010
$1.6M
NCI NIH HHS R01 CA058033NCI NIH HHS R01 CA120901NIA NIH HHS R01 AG036690
6 · The paper itself

Abstract

Defective expression of LATS2, a negative regulator of YAP oncoprotein, has been reported in cancer of prostate, breast, liver, brain, and blood origins. However, no transcriptional regulators for the LATS2 gene have been identified. Here we report that spontaneous mutation of the transcription factor FOXP3 reduces expression of the LATS2 gene in mammary epithelial cells. shRNA-mediated silencing of FOXP3 in normal or malignant mammary epithelial cells of mouse and human origin repressed LATS2 expression and increased YAP protein levels. LATS2 induction required binding of FOXP3 to a specific sequence in the LATS2 promoter, and this interaction contributed to FOXP3-mediated growth inhibition of tumor cells. In support of these results, reduced expression and somatic mutations of FOXP3 correlated strongly with defective LATS2 expression in microdissected prostate cancer tissues. Thus, defective expression of LATS2 is attributable to FOXP3 defects and may be a major independent determinant of YAP protein elevation in cancer. Our findings identify a novel mechanism of LATS2 downregulation in cancer and reveal an important tumor suppressor relay between the FOXP3 and HIPPO pathways which are widely implicated in human cancer.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingAnimalsBase SequenceBlotting, WesternBreast NeoplasmsCell Line, TumorFemaleForkhead Transcription FactorsGene Expression Regulation, NeoplasticHippo KinasesHumansImmunohistochemistryMaleMiceMice, Inbred BALB CAdaptor Proteins, Signal TransducingForkhead Transcription FactorsFOXP3 protein, humanHippo KinasesLATS2 protein, humanPhosphoproteinsProtein Serine-Threonine KinasesSerine-Threonine Kinase 3STK3 protein, humanTranscription FactorsTumor Suppressor ProteinsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID21278236
PMCPMC3070402
OpenAlexW2102064571

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.