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A comparison of the effects of Angiotensin IV on androgen-dependent and androgen-independent prostate cancer cell lines

机译:血管紧张素IV对雄激素依赖性和非雄激素依赖性前列腺癌细胞系的作用比较

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Introduction: Angiotensin IV is one of the biologically active peptides of the renin–angiotensin system. Limited data suggests that this hexapeptide could contribute to cancer development and/or progression. Materials and methods: Using the MTT reduction assay as an indicator of cell viability, and the bromodeoxyuridine incorporation assay as an indicator of cell proliferation, the influence of Angiotensin IV was evaluated on two human prostate cancer lines: androgen-dependent (LNCaP) and androgen-independent (DU-145). The potential effect of Angiotensin IV classic angiotensin receptors was examined by using the selective antagonists losartan and PD123319. Finally, the changes in expression levels of AT1 and AT2 receptors were compared, before and after angiotensin treatment. Results: Angiotensin IV caused significant changes in cell viability and proliferation in LNCaP cells but not in DU-145. It was found that AT2 receptor blocker (PD123319) was able to diminish the suppressor effect of Angiotensin IV on bromodeoxyuridine incorporation into the DNA of androgen-dependent prostate cancer cells. Simultaneously, it was reported that Angiotensin IV is the factor that modulates the density of AT1 and AT2 receptors in prostate cancer cells. Conclusions: These findings suggested that Angiotensin IV can modulate tumour cell proliferation in the early stage of androgen-dependent prostate cancer. The effect might be promoted by the change of the angiotensin receptor level.
机译:简介:血管紧张素IV是肾素-血管紧张素系统的生物活性肽之一。有限的数据表明该六肽可能有助于癌症的发展和/或进展。材料和方法:使用MTT还原法作为细胞活力的指标,而溴脱氧尿苷掺入法作为细胞增殖的指标,评估了血管紧张素IV对两种人前列腺癌株的影响:雄激素依赖性(LNCaP)和雄激素-独立(DU-145)。通过使用选择性拮抗剂氯沙坦和PD123319,检查了血管紧张素IV经典血管紧张素受体的潜在作用。最后,比较了血管紧张素治疗前后AT1和AT2受体表达水平的变化。结果:血管紧张素IV在LNCaP细胞中引起细胞活力和增殖的显着变化,但在DU-145中却没有。发现AT2受体阻断剂(PD123319)能够减弱血管紧张素IV对溴脱氧尿苷掺入雄激素依赖性前列腺癌细胞的DNA中的抑制作用。同时,据报道血管紧张素IV是调节前列腺癌细胞中AT1和AT2受体密度的因子。结论:这些发现表明血管紧张素IV可以在雄激素依赖性前列腺癌的早期调节肿瘤细胞的增殖。血管紧张素受体水平的改变可能会促进这种作用。

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