Journal ArticleDOI
Stimulation of the bradykinin B(1) receptor induces the proliferation of estrogen-sensitive breast cancer cells and activates the ERK1/2 signaling pathway.
Luis Molina,Carola E. Matus,Angel Astroza,Francisca Pavicic,Eugenio Tapia,Cesar Toledo,Pérez Ja,Francisco Nualart,Carlos B. Gonzalez,Rafael A. Burgos,Carlos D. Figueroa,Pamela Ehrenfeld,María Teresa Poblete +12 more
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TLDR
The capacity of B1R to trigger cell proliferation in breast cancer cells is investigated, some of the downstream events occurring after B 1R stimulation that may be linked to cell proliferation are explored, and whether human breast tumors express potentially active B1 R assessed by the binding of a radiolabeled agonist is determined.Abstract:
Kinin peptides exert multiple biological effects by binding to two types of G protein-coupled receptors known as B(1) (B(1)R) and B(2) receptors. Expression of the B(1)R in human breast cancer was recently reported, but up to now the consequences of its stimulation are unknown. Our aims were (1) to investigate the capacity of B(1)R to trigger cell proliferation in breast cancer cells, (2) to explore some of the downstream events occurring after B(1)R stimulation that may be linked to cell proliferation, and (3) to determine whether human breast tumors express potentially active B(1)R assessed by the binding of a radiolabeled agonist. Breast cancer cells expressed both the mRNA and the immunoreactive protein of B(1)R that once stimulated triggered cell proliferation at nanomolar concentrations of the ligand. Inhibitor studies suggested that the proliferative effects depend on the activity of epidermal growth factor receptor and subsequent ERK1/2 mitogen-activated protein kinases phosphorylation. B(1)R binding sites, were detected in 3/4 fibroadenomas, in 4/4 ductal carcinomas in situ and in 11/13 invasive ductal carcinomas. The B(1)R-epidermal growth factor receptor crosstalk may be a key interaction that maintains tumor growth, and antagonism of B(1)R may be a valuable alternative for the treatment of breast cancer.read more
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The role of kinin receptors in cancer and therapeutic opportunities
TL;DR: Evidence supports the concept that kinin receptors, especially kinin receptor 1, are promising targets for cancer therapy, and it is expected that B1R antagonists would interfere less with housekeeping functions and therefore would be attractive compounds to treat selected types of cancer.
Journal ArticleDOI
GPCRs and cancer
TL;DR: A broad overview on the biological activity elicited by GPCRs in tumor cells and the molecular mechanisms by which these receptors exert a primary action in cancer progression are provided to contribute to the identification of novel pharmacological approaches for cancer patients.
Journal ArticleDOI
Different cross-talk sites between the renin-angiotensin and the kallikrein-kinin systems.
TL;DR: Cross-talks explain why both the RAS and KKS are up-regulated in some circumstances, whereas in other circumstances both systems change in the opposite manner.
Journal ArticleDOI
GPER-1/GPR30 a novel estrogen receptor sited in the cell membrane: therapeutic coupling to breast cancer
TL;DR: The discovery of GPER-1 as a novel estrogen receptor is unique and the signaling pathways activated by its stimulation indicate a potential role of GP ER-1 in the genesis and mechanisms of drug resistance in breast cancer.
Journal ArticleDOI
Bradykinin enhances cell migration in human chondrosarcoma cells through BK receptor signaling pathways
Wei Hung Yang,Jung Tzu Chang,Sheng Feng Hsu,Te-Mao Li,Der Yang Cho,Chun-Yin Huang,Yi-Chin Fong,Chih-Hsin Tang +7 more
TL;DR: Results indicated that BK enhances the migration of chondrosarcoma cells by increasing α2β1 integrin expression through the BK receptors/PLC/PKCδ/NF‐κB signal transduction pathway.
References
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Journal ArticleDOI
International Union of Pharmacology: Approaches to the Nomenclature of Voltage-Gated Ion Channels
William A. Catterall,K. G. Chandy,David E. Clapham,George A. Gutman,Franz Hofmann,Anthony J. Harmar,Darrell R. Abernethy,Michael Spedding +7 more
TL;DR: This issue of Pharmacological Reviews includes a new venture in the collaboration between the International Union of Pharmacology (IUPHAR) and the American Society for Pharmacology and Experimental Therapeutics (ASPET), in that a new classification of voltage-gated ion channels is outlined.
Journal Article
Bioregulation of kinins: kallikreins, kininogens, and kininases.
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International Union of Pharmacology. XLV. Classification of the Kinin Receptor Family: from Molecular Mechanisms to Pathophysiological Consequences
L. M. Fredrik Leeb-Lundberg,François Marceau,Werner Müller-Esterl,Douglas J. Pettibone,Bruce L. Zuraw +4 more
TL;DR: This review is a comprehensive presentation of the current understanding of B1 and B2 receptors in terms of molecular and cell biology, physiology, pharmacology, and involvement in human disease and drug development.
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Host microenvironment in breast cancer development: inflammatory cells, cytokines and chemokines in breast cancer progression: reciprocal tumor-microenvironment interactions.
TL;DR: The purpose of the present review is to outline the reciprocal interactions that exist between these different elements, and to shed light on their potential involvement in breast cancer development and progression.
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Activation of mitogen-activated protein kinase in estrogen receptor α-positive breast cancer cells in vitro induces an in vivo molecular phenotype of estrogen receptor α-negative human breast tumors
Chad J. Creighton,Amy Hilger,Shalini Murthy,James M. Rae,Arul M. Chinnaiyan,Dorraya El-Ashry +5 more
TL;DR: The results confirm that increased MAPK activation causes loss of ERalpha expression and suggest that hyperactivation of MAPK plays a role in the generation of the ERalpha- phenotype in breast cancer.