Evidence map›Paper›PMID 27294705›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Suppression of KSHV-induced angiopoietin-2 inhibits angiogenesis, infiltration of inflammatory cells, and tumor growth.

Xiaolan Yu, Jingfeng Sha, Shao Xiang, Sanhai Qin, Patricia Conrad, Santosh K Ghosh, Aaron Weinberg, Fengchun Ye

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Clinical relevance of tumour-associated macrophages.Nature reviews. Clinical oncology · 2022
    Review
  6. Review
  7. Review
  8. Hedgehog Signaling: Implications in Cancers and Viral Infections.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. 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

8 authors at 1 institution in 2 countries.

Xiaolan Yua Department of Biological Sciences , School of Dental Medicine, Case Western Reserve University , Cleveland , OH , USA.
Jingfeng Shaa Department of Biological Sciences , School of Dental Medicine, Case Western Reserve University , Cleveland , OH , USA.
Shao Xianga Department of Biological Sciences , School of Dental Medicine, Case Western Reserve University , Cleveland , OH , USA.
Sanhai Qina Department of Biological Sciences , School of Dental Medicine, Case Western Reserve University , Cleveland , OH , USA.
Patricia Conradc Department of Genetics , School of Medicine, Case Western Reserve University , Cleveland , OH , USA.
Santosh K Ghosha Department of Biological Sciences , School of Dental Medicine, Case Western Reserve University , Cleveland , OH , USA.
Aaron Weinberga Department of Biological Sciences , School of Dental Medicine, Case Western Reserve University , Cleveland , OH , USA.
Fengchun Yea Department of Biological Sciences , School of Dental Medicine, Case Western Reserve University , Cleveland , OH , USA.
Case Western Reserve University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kaposi's sarcoma (KS) is a highly angiogenic and inflammatory neoplasia. The angiogenic and inflammatory cytokine angiopoietin-2 (Ang-2) is strongly expressed in KS due to Kaposi's sarcoma-associated herpesvirus (KSHV) infection. In the present study, we determined how Ang-2 contributes to development of KS by using telomerase-immortalized human umbilical vein endothelial cells (TIVE) as a model, which become malignantly transformed and express increased levels of Ang-2 following KSHV infection. Ang-2 released from TIVE-KSHV cells induces tyrosine phosphorylation of Tie-2 receptor from both human and mouse endothelial cells and promotes angiogenesis in nude mice. Functional inhibition or expressional "knock-down" of Ang-2 in these cells blocks angiogenesis and inhibits tumor growth. Ang-2 suppression also reduces the numbers of infiltrating monocytes/macrophages in tumors. In transwell-based cell migration assays, Ang-2 indeed enhances migration of human monocytes in a dose-dependent manner. These results underscore a pivotal role of KSHV-induced Ang-2 in KS tumor development by promoting both angiogenesis and inflammation. Our data also suggest that selective drug targeting of Ang-2 may be used for treatment of KS.

Indexed as

Angiopoietin-2AnimalsCell MovementCell ProliferationGene Knockdown TechniquesHerpesvirus 8, HumanHumansHuman Umbilical Vein Endothelial CellsInflammationMacrophagesMice, NudeMonocytesNeoplasmsNeovascularization, PathologicPhosphorylationReceptor, TIE-2Angiopoietin-2Receptor, TIE-2Recombinant Fusion ProteinsTelomerasetrebananiband Kaposi's sarcomaangiogenesisangiopoietin-2inflammationKSHV

Identifiers

PMID27294705
PMCPMC4968962
OpenAlexW2432616534

What OpenQuestion holds

Textmetadata
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.