Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/17435
Title: The kallikrein-Kinin system modulates the progression of colorectal liver metastases in a mouse model.
Authors: da Costa, Patricia LN;Wynne, David;Fifis, Theodora;Nguyen, Linh;Perini, Marcos V;Christophi, Christopher
Affiliation: Department of Surgery, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
Laboratório de Oncologia Experimental, Faculdade de Medicina da Universidade de São Paulo and Instituto do Câncer do Estado de São Paulo, São Paulo, Brazil
Issue Date: 4-Apr-2018
Citation: BMC cancer 2018; 18(1): 382
Abstract: The 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. B1R 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. Both 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. Taken 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.
URI: http://ahro.austin.org.au/austinjspui/handle/1/17435
DOI: 10.1186/s12885-018-4260-6
ORCID: 0000-0002-4143-5225
PubMed URL: 29618333
Type: Journal Article
Subjects: Bradykinin receptor
Colorectal liver metastases
Kallikrein-Kinin system
Kinin or bradykinin
Appears in Collections:Journal articles

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