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首页> 外文期刊>Journal of Cellular Physiology >Angiotensin II/angiotensin II type I receptor (AT1R) signaling promotes MCF-7 breast cancer cells survival via PI3-kinase/Akt pathway.
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Angiotensin II/angiotensin II type I receptor (AT1R) signaling promotes MCF-7 breast cancer cells survival via PI3-kinase/Akt pathway.

机译：血管紧张素ⅱ/血管紧张素ⅱ1型受体(AT1R)信号促进MCF-7乳腺癌细胞生存通过pi3激酶/ Akt通路。

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摘要

Angiotensin II (Ang II) is a bioactive peptide of the renin-angiotensin system, acting not only as a vasoconstrictor but also as a growth promoter via angiotensin II type 1 receptor (AT1R) in some cancer. In this study, we examined the mechanisms by which Ang II affected the cell proliferation in AT1R-positive MCF-7 human breast cancer cells. Ang II stimulated the growth of breast cancer cells in a dose- and time-dependent manner. The maximal proliferation effect on MCF-7 cells was obtained with 10(-4) M Ang II at 24 h. Losartan (10(-5) M, an AT1R antagonist) significantly decreased the level of Ang-II-induced proliferative effects, whereas PD123319 (10(-5) M, an AT2R antagonist) had no effects. Moreover, Ang II could significantly accelerate S-phase progression, which was inhibited by losartan (10(-5) M) or LY294002 (50 microM, a PI3-kinase inhibitor). In addition, Ang II caused rapid activation of p-Akt in a dose- and time-dependent manner. 10(-4) M Ang II induced a significant increase of p-Akt in 15 min. The peak level of p-Akt could be persisted for at least 6 h. Among the signaling molecules downstream of Akt, we revealed that Ang II also significantly upregulated CyclinD1, GSK3beta, and downregulated p27. Pretreatment with losartan (10(-5) M) or LY294002 (50 microM) could significantly suppress these effects of Ang II. These findings suggest that Ang II plays a role in the growth of AT1R-positive breast cancer cells through PI3-kinase/Akt pathway activation. Therefore, targeting Ang II/AT1R signaling could be a novel therapeutic for breast cancer.
机译：血管紧张素ⅱ(Angⅱ)是一种生物活性肽肾素-血管紧张素系统,不仅扮演血管收缩剂也作为生长促进剂通过血管紧张素ⅱ1型受体(AT1R)在一些癌症。和二世对细胞增殖的影响在AT1R-positive MCF-7人类乳腺癌细胞。Angⅱ刺激乳腺癌的生长细胞的剂量和时间的方式。最大对MCF-7细胞增殖的影响获得10 (4)M Angⅱ在24 h。洛沙坦(10 (5) M, AT1R拮抗剂)Ang-II-induced水平下降增殖的影响,而PD123319 (10 (5)米,一个AT2R拮抗剂)没有影响。Angⅱ可以显著加速s阶段进展,被洛沙坦(10(5)米)或LY294002 (50 microM pi3激酶抑制剂)。激活p-Akt的剂量和时间的方式。增加p-Akt 15分钟的峰值水平p-Akt可以持续至少6 h。一种蛋白激酶的下游信号分子,我们显示和二世也显著调节CyclinD1、GSK3beta和表达下调p27。LY294002 (50 microM)可以显著抑制这些影响和二世。和二世在增长的过程中发挥作用AT1R-positive乳腺癌细胞pi3激酶/ Akt通路激活。针对Angⅱ/ AT1R信号可能是小说治疗乳腺癌。

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