Evidence map›Paper›PMID 32541784›Full record

ArticleNature communications2020

Dual Role of WISP1 in maintaining glioma stem cells and tumor-supportive macrophages in glioblastoma.

Weiwei Tao, Chengwei Chu, Wenchao Zhou, Zhi Huang, Kui Zhai, Xiaoguang Fang, Qian Huang, Aili Zhang, Xiuxing Wang, Xingjiang Yu and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
8.8field-weighted citation impact, top 1% 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

117 citing papers in PubMed, 181 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

57 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

18 authors at 4 institutions in 1 country.

Weiwei TaoDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Chengwei ChuDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Wenchao ZhouDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Zhi HuangDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Kui ZhaiDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Xiaoguang FangDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Qian HuangDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Aili ZhangDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Xiuxing WangDivision of Regenerative Medicine, Department of Medicine, University of California, San Diego, San Diego, CA, 92037, USA.
Xingjiang YuDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Haidong HuangDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Qiulian WuDivision of Regenerative Medicine, Department of Medicine, University of California, San Diego, San Diego, CA, 92037, USA.
Andrew E SloanBrain Tumor and Neuro-Oncology Center, Seidman Cancer Center, University Hospitals, Case Western Reserve University, Cleveland, OH, 44106, USA.
Jennifer S YuDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Xiaoxia LiCase Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, OH, 44106, USA.ORCID http://orcid.org/0000-0002-4872-9525
George R StarkDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Jeremy N RichDivision of Regenerative Medicine, Department of Medicine, University of California, San Diego, San Diego, CA, 92037, USA.ORCID http://orcid.org/0000-0001-7845-5302
Shideng BaoDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA. baos@ccf.org.ORCID http://orcid.org/0000-0002-4236-2662
Cleveland Clinic Lerner College of Medicine · USUniversity of California San Diego · USCleveland Clinic · USUniversity Hospitals Seidman Cancer Center · US

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Jesse Nodora · 1985 to 2026
$124.9M
Glioblastoma stem cell-derived pericytes and cancer invasionR01NS091080 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI BAO, SHIDENG · 2016 to 2020
$1.7M
Ubiquitination and Deubiquitination of c-Myc in GlioblastomaR01NS099175 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI BAO, SHIDENG · 2016 to 2020
$1.7M
PerkinElmer IVIS Spectrum CTS10OD018205 · OD · CLEVELAND CLINIC LERNER COM-CWRU · PI DRAZBA, JUDY · 2015 to 2015
$600k
NCI NIH HHS P30 CA023100NIH HHS S10 OD018205NINDS NIH HHS R01 NS091080NINDS NIH HHS R01 NS099175
6 · The paper itself

Abstract

The interplay between glioma stem cells (GSCs) and the tumor microenvironment plays crucial roles in promoting malignant growth of glioblastoma (GBM), the most lethal brain tumor. However, the molecular mechanisms underlying this crosstalk are incompletely understood. Here, we show that GSCs secrete the Wnt-induced signaling protein 1 (WISP1) to facilitate a pro-tumor microenvironment by promoting the survival of both GSCs and tumor-associated macrophages (TAMs). WISP1 is preferentially expressed and secreted by GSCs. Silencing WISP1 markedly disrupts GSC maintenance, reduces tumor-supportive TAMs (M2), and potently inhibits GBM growth. WISP1 signals through Integrin α6β1-Akt to maintain GSCs by an autocrine mechanism and M2 TAMs through a paracrine manner. Importantly, inhibition of Wnt/β-catenin-WISP1 signaling by carnosic acid (CA) suppresses GBM tumor growth. Collectively, these data demonstrate that WISP1 plays critical roles in maintaining GSCs and tumor-supportive TAMs in GBM, indicating that targeting Wnt/β-catenin-WISP1 signaling may effectively improve GBM treatment and the patient survival.

Indexed as

AnimalsBrain NeoplasmsCCN Intercellular Signaling ProteinsCell Line, TumorCell ProliferationDoxycyclineGliomaHumansKaplan-Meier EstimateMacrophagesMice, Inbred NODMice, KnockoutMice, SCIDNeoplastic Stem CellsProto-Oncogene ProteinsProto-Oncogene Proteins c-aktCCN4 protein, humanCCN Intercellular Signaling ProteinsDoxycyclineProto-Oncogene ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID32541784
PMCPMC7295765
OpenAlexW3034391615

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.