Evidence map›Paper›PMID 28427524›Full record

ReviewCritical reviews in oncology/hematology2017

Kallistatin suppresses cancer development by multi-factorial actions.

Julie Chao, Pengfei Li, Lee Chao

Abstract readReview
In one paragraph

Review in Critical reviews in oncology/hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  7. TheInternational journal of women's health · 2021
    Article
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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

3 authors at 1 institution in 1 country.

Julie ChaoDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA. Electronic address: chaoj@musc.edu.
Pengfei LiDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA.
Lee ChaoDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA.
Medical University of South Carolina · US

Funding

Kallistatin in Vascular InjuryR01HL118516 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CHAO, JULIE · 2014 to 2017
$1.5M
NHLBI NIH HHS R01 HL118516
6 · The paper itself

Abstract

Kallistatin was first identified in human plasma as a tissue kallikrein-binding protein and a serine proteinase inhibitor. Kallistatin via its two structural elements regulates differential signaling cascades, and thus a wide spectrum of biological functions. Kallistatin's active site is essential for: inhibiting tissue kallikrein's activity; stimulating endothelial nitric oxide synthase and sirtuin 1 expression and activation; and modulating the synthesis of the microRNAs, miR-34a, miR-21 and miR-203. Kallistatin's heparin-binding site is crucial for antagonizing the signaling pathways of vascular endothelial growth factor, tumor necrosis factor-α, Wnt, transforming growth factor-β and epidermal growth factor. Circulating kallistatin levels are markedly reduced in patients with prostate and colon cancer. Kallistatin administration attenuates angiogenesis, inflammation, tumor growth and invasion in animal models and cultured cells. Therefore, tumor progression may be substantially suppressed by kallistatin's pleiotropic activities. In this review, we will discuss the role and mechanisms of kallistatin in the regulation of cancer development.

Indexed as

Antineoplastic AgentsDisease ProgressionFemaleHumansInflammationMaleMicroRNAsNeoplasmsNeovascularization, PathologicSerpinsSignal TransductionAntineoplastic AgentskallistatinMicroRNAsSerpinsAngiogenesisApoptosisCancerHyperoxiaInflammationKallistatinVascular endothelial growth factor

Identifiers

PMID28427524
PMCPMC5441310
OpenAlexW2596111027

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.