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Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture.
J Endocrinol. 2005 Aug; 186(2):291-301.JE

Abstract

We have previously reported that bradykinin (BK) represents an influential mitogenic agent in normal breast glandular tissue. We here investigated the mitogenic effects and the signalling pathways of BK in primary cultured human epithelial breast cells obtained from a tumour and from the histologically proven non-malignant tissue adjacent to the tumour. BK provoked cell proliferation, increase in cytosolic calcium, activation of protein kinase C (PKC)-alpha, -beta, -delta, -epsilon and -eta and phosphorylation of the extracellular-regulated kinases 1 and 2 (ERK1/2). The following compounds blocked the proliferative effects of BK: Hyp3-BK, a B2 receptor subtype inhibitor; U73122, a phospholipase C-beta inhibitor; GF109203X, a protein kinase C (PKC) inhibitor; and PD98059, a mitogen-activated protein kinase kinase inhibitor. Gö6976, a Ca(2+)-dependent PKC inhibitor, did not have any effect. In conclusion, the mitogenic effects of BK are retained in peritumour and tumour cells; hence, it is likely that BK has an important role in cancer endorsement and progression.

Authors+Show Affiliations

Department of Biological and Environmental Sciences and Technologies, Ecotekne, Università di Lecce, Monteroni, Via Provinciale per Monteroni, 73100 Lecce, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16079255

Citation

Greco, S, et al. "Bradykinin Stimulates Cell Proliferation Through an Extracellular-regulated Kinase 1 and 2-dependent Mechanism in Breast Cancer Cells in Primary Culture." The Journal of Endocrinology, vol. 186, no. 2, 2005, pp. 291-301.
Greco S, Elia MG, Muscella A, et al. Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture. J Endocrinol. 2005;186(2):291-301.
Greco, S., Elia, M. G., Muscella, A., Romano, S., Storelli, C., & Marsigliante, S. (2005). Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture. The Journal of Endocrinology, 186(2), 291-301.
Greco S, et al. Bradykinin Stimulates Cell Proliferation Through an Extracellular-regulated Kinase 1 and 2-dependent Mechanism in Breast Cancer Cells in Primary Culture. J Endocrinol. 2005;186(2):291-301. PubMed PMID: 16079255.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture. AU - Greco,S, AU - Elia,M G, AU - Muscella,A, AU - Romano,S, AU - Storelli,C, AU - Marsigliante,S, PY - 2005/8/5/pubmed PY - 2005/9/24/medline PY - 2005/8/5/entrez SP - 291 EP - 301 JF - The Journal of endocrinology JO - J. Endocrinol. VL - 186 IS - 2 N2 - We have previously reported that bradykinin (BK) represents an influential mitogenic agent in normal breast glandular tissue. We here investigated the mitogenic effects and the signalling pathways of BK in primary cultured human epithelial breast cells obtained from a tumour and from the histologically proven non-malignant tissue adjacent to the tumour. BK provoked cell proliferation, increase in cytosolic calcium, activation of protein kinase C (PKC)-alpha, -beta, -delta, -epsilon and -eta and phosphorylation of the extracellular-regulated kinases 1 and 2 (ERK1/2). The following compounds blocked the proliferative effects of BK: Hyp3-BK, a B2 receptor subtype inhibitor; U73122, a phospholipase C-beta inhibitor; GF109203X, a protein kinase C (PKC) inhibitor; and PD98059, a mitogen-activated protein kinase kinase inhibitor. Gö6976, a Ca(2+)-dependent PKC inhibitor, did not have any effect. In conclusion, the mitogenic effects of BK are retained in peritumour and tumour cells; hence, it is likely that BK has an important role in cancer endorsement and progression. SN - 0022-0795 UR - https://www.unboundmedicine.com/medline/citation/16079255/Bradykinin_stimulates_cell_proliferation_through_an_extracellular_regulated_kinase_1_and_2_dependent_mechanism_in_breast_cancer_cells_in_primary_culture_ L2 - https://joe.bioscientifica.com/doi/10.1677/joe.1.06052 DB - PRIME DP - Unbound Medicine ER -