Tags

Type your tag names separated by a space and hit enter

Angiotensin II activates extracellular signal regulated kinases via protein kinase C and epidermal growth factor receptor in breast cancer cells.
J Cell Physiol. 2003 Aug; 196(2):370-7.JC

Abstract

Angiotensin II (Ang II) induces, through AT1, intracellular Ca(2+) increase in both normal and cancerous breast cells in primary culture (Greco et al., 2002 Cell Calcium 2:1-10). We here show that Ang II stimulated, in a dose-dependent manner, the 24 h-proliferation of breast cancer cells in primary culture, induced translocation of protein kinase C (PKC)-alpha, -beta1/2, and delta (but not -epsilon, -eta, -theta, -zeta, and -iota), and phosphorylated extracellular-regulated kinases 1 and 2 (ERK1/2). The proliferative effects of Ang II were blocked by the AT1 antagonist, losartan. Also epidermal growth factor (EGF) had mitogenic effects on serum-starved breast cancer cells since induced cell proliferation after 24 h and phosphorylation of ERK1/2. The Ang II-induced proliferation of breast cancer cells was reduced by (a) Gö6976, an inhibitor of conventional PKC-alpha and -beta1, (b) AG1478, an inhibitor of the tyrosine kinase of the EGF receptor (EGFR), and (c) downregulation of 1,2-diacylglycerol-sensitive PKCs achieved by phorbol 12-myristate 13-acetate (PMA). A complete inhibition of the Ang II-induced cell proliferation was achieved using the inhibitor of the mitogen activated protein kinase kinase (MAPKK or MEK), PD098059, or using Gö6976 together with AG1478. These results indicate that in human primary cultured breast cancer cells AT1 regulates mitogenic signaling pathways by two simultaneous mechanisms, one involving conventional PKCs and the other EGFR transactivation.

Authors+Show Affiliations

Laboratory of Cell Physiology, Dipartimento di Scienze e Tecnologie Biologiche e Ambientali, University of Lecce, Ecotekne, Lecce, Italy.No affiliation info availableNo affiliation info availableNo 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

12811831

Citation

Greco, S, et al. "Angiotensin II Activates Extracellular Signal Regulated Kinases Via Protein Kinase C and Epidermal Growth Factor Receptor in Breast Cancer Cells." Journal of Cellular Physiology, vol. 196, no. 2, 2003, pp. 370-7.
Greco S, Muscella A, Elia MG, et al. Angiotensin II activates extracellular signal regulated kinases via protein kinase C and epidermal growth factor receptor in breast cancer cells. J Cell Physiol. 2003;196(2):370-7.
Greco, S., Muscella, A., Elia, M. G., Salvatore, P., Storelli, C., Mazzotta, A., Manca, C., & Marsigliante, S. (2003). Angiotensin II activates extracellular signal regulated kinases via protein kinase C and epidermal growth factor receptor in breast cancer cells. Journal of Cellular Physiology, 196(2), 370-7.
Greco S, et al. Angiotensin II Activates Extracellular Signal Regulated Kinases Via Protein Kinase C and Epidermal Growth Factor Receptor in Breast Cancer Cells. J Cell Physiol. 2003;196(2):370-7. PubMed PMID: 12811831.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin II activates extracellular signal regulated kinases via protein kinase C and epidermal growth factor receptor in breast cancer cells. AU - Greco,S, AU - Muscella,A, AU - Elia,M G, AU - Salvatore,P, AU - Storelli,C, AU - Mazzotta,A, AU - Manca,C, AU - Marsigliante,S, PY - 2003/6/18/pubmed PY - 2003/8/12/medline PY - 2003/6/18/entrez SP - 370 EP - 7 JF - Journal of cellular physiology JO - J. Cell. Physiol. VL - 196 IS - 2 N2 - Angiotensin II (Ang II) induces, through AT1, intracellular Ca(2+) increase in both normal and cancerous breast cells in primary culture (Greco et al., 2002 Cell Calcium 2:1-10). We here show that Ang II stimulated, in a dose-dependent manner, the 24 h-proliferation of breast cancer cells in primary culture, induced translocation of protein kinase C (PKC)-alpha, -beta1/2, and delta (but not -epsilon, -eta, -theta, -zeta, and -iota), and phosphorylated extracellular-regulated kinases 1 and 2 (ERK1/2). The proliferative effects of Ang II were blocked by the AT1 antagonist, losartan. Also epidermal growth factor (EGF) had mitogenic effects on serum-starved breast cancer cells since induced cell proliferation after 24 h and phosphorylation of ERK1/2. The Ang II-induced proliferation of breast cancer cells was reduced by (a) Gö6976, an inhibitor of conventional PKC-alpha and -beta1, (b) AG1478, an inhibitor of the tyrosine kinase of the EGF receptor (EGFR), and (c) downregulation of 1,2-diacylglycerol-sensitive PKCs achieved by phorbol 12-myristate 13-acetate (PMA). A complete inhibition of the Ang II-induced cell proliferation was achieved using the inhibitor of the mitogen activated protein kinase kinase (MAPKK or MEK), PD098059, or using Gö6976 together with AG1478. These results indicate that in human primary cultured breast cancer cells AT1 regulates mitogenic signaling pathways by two simultaneous mechanisms, one involving conventional PKCs and the other EGFR transactivation. SN - 0021-9541 UR - https://www.unboundmedicine.com/medline/citation/12811831/Angiotensin_II_activates_extracellular_signal_regulated_kinases_via_protein_kinase_C_and_epidermal_growth_factor_receptor_in_breast_cancer_cells_ L2 - https://doi.org/10.1002/jcp.10313 DB - PRIME DP - Unbound Medicine ER -