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首页> 外文期刊>Journal of Cellular Physiology >Angiotensin II activates extracellular signal regulated kinases via protein kinase C and epidermal growth factor receptor in breast cancer cells.
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Angiotensin II activates extracellular signal regulated kinases via protein kinase C and epidermal growth factor receptor in breast cancer cells.

机译：血管紧张素ⅱ激活细胞外信号通过蛋白激酶C和调节激酶表皮生长因子受体在乳腺癌细胞。

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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 - varepsilon, -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) Go6976, 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 Go6976 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. J. Cell. Physiol. 196: 370-377, 2003.
机译：血管紧张素ⅱ(Angⅱ)诱导,通过AT1、细胞内钙(2 +)在正常和增加癌乳腺癌细胞在初级(希腊文化细胞钙2:1-10 et al ., 2002)。Angⅱ刺激,存在剂量依赖的相关性方式,24 h-proliferation乳腺癌细胞的主要文化、诱导易位蛋白激酶C (PKC) t1, -beta1/2,δ(但不是——varepsilon埃塔,θ,ζ,和极微小),磷酸化extracellular-regulated激酶1和2 (ERK1/2)。的增殖的影响和二世被封锁AT1拮抗剂,洛沙坦。生长因子(EGF)促有丝分裂的影响serum-starved自诱导乳腺癌细胞细胞增殖后24 h和磷酸化ERK1/2。乳腺癌细胞降低了Go6976(一个),一个抑制剂的常规PKC-alpha beta1,(b) AG1478,酪氨酸激酶的抑制剂表皮生长因子受体(EGFR)和(c)2-diacylglycerol-sensitive downregulation 1PKCs通过佛波醇12-myristate 13-acetate(PMA)。II-induced细胞增殖是通过使用有丝分裂原激活蛋白的抑制剂PD098059激酶激酶(MAPKK或MEK),或使用Go6976 AG1478一起。表明在人类主要讲究的乳房癌细胞AT1调节促有丝分裂的信号路径由两个同步机制,一个涉及传统的PKCs和表皮生长因子受体transactivation。2003.

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