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VIP-ellipticine derivatives inhibit the growth of breast cancer cells.

机译:VIP-玫瑰树碱衍生物抑制乳腺癌细胞的生长。

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摘要

The effects of vasoactive intestinal peptide (VIP)-ellipticine (E) derivatives were investigated on breast cancer cells. VIP-ALALA-E and VIP-LALA-E inhibited 125I-VIP binding to MCF-7 cells with an IC(50) values of 1 and 0.2 microM respectively. VIP-ALALA-E and VIP-LALA-E caused elevation of cAMP in MCF-7 cells with ED(50) values of 1 and 0.1 microM. VIP-LALA-E caused increased c-fos mRNA in MCF-7 cells. Radiolabeled VIP-LALA-E was internalized at 37 degrees C and delivered the cytotoxic E into MCF-7 cells. VIP-LALA-E inhibited the clonal growth of MCF-7 cells, decreased cell viability based on trypan blue exclusion and reduced 35S-methionine uptake. These results indicate that VIP-E derivatives function as breast cancer VPAC(1) receptor agonists which inhibit MCF-7 cellular viability.
机译:研究了血管活性肠肽(VIP)-玫瑰树碱(E)衍生物对乳腺癌细胞的作用。 VIP-ALALA-E和VIP-LALA-E抑制125I-VIP与MCF-7细胞的结合,IC(50)值分别为1和0.2 microM。 VIP-ALALA-E和VIP-LALA-E导致MCF-7细胞中cAMP升高,ED(50)值为1和0.1 microM。 VIP-LALA-E导致MCF-7细胞中c-fos mRNA增加。放射性标记的VIP-LALA-E在37摄氏度下被内化,并将细胞毒性E传递到MCF-7细胞中。 VIP-LALA-E抑制MCF-7细胞的克隆生长,基于锥虫蓝排除作用降低了细胞活力,并降低了35S-蛋氨酸的摄取。这些结果表明VIP-E衍生物起抑制MCF-7细胞生存力的乳腺癌VPAC(1)受体激动剂的作用。

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