Evidence map›Paper›PMID 29618333›Full record

ArticleBMC cancer2018

The kallikrein-Kinin system modulates the progression of colorectal liver metastases in a mouse model.

Patricia Luiza Nunes da Costa, David Wynne, Theodora Fifis, Linh Nguyen, Marcos Perini, Christopher Christophi

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.2field-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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Factor XII-A New Therapeutic Target? A Systematic Review.International journal of molecular sciences · 2026
    Pooled it
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  5. PMToxics · 2024
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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

6 authors at 3 institutions in 2 countries.

Patricia Luiza Nunes da CostaDepartment of Surgery, University of Melbourne, Austin Health, Lance Townsend Building Level 8, Studley Rd, Heidelberg, VIC, 3084, Australia.
David WynneDepartment of Surgery, University of Melbourne, Austin Health, Lance Townsend Building Level 8, Studley Rd, Heidelberg, VIC, 3084, Australia.
Theodora FifisDepartment of Surgery, University of Melbourne, Austin Health, Lance Townsend Building Level 8, Studley Rd, Heidelberg, VIC, 3084, Australia. tfifis@unimelb.edu.au.
Linh NguyenDepartment of Surgery, University of Melbourne, Austin Health, Lance Townsend Building Level 8, Studley Rd, Heidelberg, VIC, 3084, Australia.
Marcos PeriniDepartment of Surgery, University of Melbourne, Austin Health, Lance Townsend Building Level 8, Studley Rd, Heidelberg, VIC, 3084, Australia.
Christopher ChristophiDepartment of Surgery, University of Melbourne, Austin Health, Lance Townsend Building Level 8, Studley Rd, Heidelberg, VIC, 3084, Australia.
Austin Health · AUInstituto do Câncer do Estado de São Paulo · BRUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Kallikrein-Kinin System (KKS) has been found to play a role in tumor progression in several cancers. The KKS metabolic cascade depends on signalling through two cross talking receptors; bradykinin receptor 1 (B1R) and bradykinin receptor 2 (B2R). Activation of the Kinin receptor is responsible for multiple pathophysiologic functions including increase of vascular permeability and induction of host inflammatory responses that exert diverse effects on tumor growth.

methodsB1R and B2R expression on mouse and human CRC cell lines was investigated. Changes in tumor growth and progression was assessed in male CBA mice bearing colorectal liver metastases (CRLM) following treatment with B1R or B2R blockers. In vitro cultures of human SW-480 and mouse colorectal cancer (MoCR) cell lines were examined for changes in their proliferation and migration properties following treatment with B1R or B2R blockers.

resultsBoth colorectal cancer cell lines tested strongly positive for B1R and B2R expression. Inhibition of both receptors retarded tumor growth but only B1R blockade significantly reduced tumor load and increased tumor apoptosis. Blockade of either receptor reduced tumor vascularization in vivo and significantly inhibited proliferation and migration of colorectal cancer cells in vitro.

conclusionTaken together, the present study demonstrated that kinin receptor blockade inhibited tumor growth and reduced its invading properties suggesting that KKS manipulation could be a novel target in colorectal cancer therapy.

Indexed as

Kallikrein-Kinin SystemAnimalsApoptosisBradykinin Receptor AntagonistsCell MovementCell ProliferationColorectal NeoplasmsDisease Models, AnimalDisease ProgressionHumansMaleMiceNeoplasm MetastasisNeoplasm StagingNeovascularization, PathologicReceptor, Bradykinin B1Bradykinin Receptor AntagonistsReceptor, Bradykinin B1Receptor, Bradykinin B2Bradykinin receptorColorectal liver metastasesKallikrein-Kinin systemKinin or bradykinin

Identifiers

PMID29618333
PMCPMC5885419
OpenAlexW2802700419

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.