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新型 GnRH 类似物与米托蒽醌偶联物对卵巢癌细胞的细胞毒性作用。

Cytotoxic Activity of Novel GnRH Analogs Conjugated with Mitoxantrone in Ovarian Cancer Cells.

机构信息

Department of Pharmacology, School of Medicine, University of Crete, 70013 Heraklion, Greece.

Department of Chemistry, University of Patras, 26504 Rion, Greece.

出版信息

Molecules. 2024 Aug 30;29(17):4127. doi: 10.3390/molecules29174127.

Abstract

The gonadotropin-releasing hormone (GnRH) receptor (GnRH-R) is highly expressed in ovarian cancer cells (OCC), and it is an important molecular target for cancer therapeutics. To develop a new class of drugs targeting OCC, we designed and synthesized Con-3 and Con-7 which are novel high-affinity GnRH-R agonists, covalently coupled through a disulfide bond to the DNA synthesis inhibitor mitoxantrone. We hypothesized that Con-3 and Con-7 binding to the GnRH-R of OCC would expose the conjugated mitoxantrone to the cellular thioredoxin, which reduces the disulfide bond of Con-3 and Con-7. The subsequent release of mitoxantrone leads to its intracellular accumulation, thus exerting its cytotoxic effects. To test this hypothesis, we determined the cytotoxic effects of Con-3 and Con-7 using the SKOV-3 human OCC. Treatment with Con-3 and Con-7, but not with their unconjugated GnRH counterparts, resulted in the accumulation of mitoxantrone within the SKOV-3 cells, increased their apoptosis, and reduced their proliferation, in a dose- and time-dependent manner, with half-maximal inhibitory concentrations of 0.6-0.9 µM. It is concluded that Con-3 and Con-7 act as cytotoxic "prodrugs" in which mitoxantrone is delivered in a GnRH-R-specific manner and constitute a new class of lead compounds for use as anticancer drugs targeting ovarian tumors.

摘要

促性腺激素释放激素(GnRH)受体(GnRH-R)在卵巢癌细胞(OCC)中高度表达,是癌症治疗的重要分子靶标。为了开发针对 OCC 的新型药物,我们设计并合成了 Con-3 和 Con-7,它们是新型高亲和力 GnRH-R 激动剂,通过二硫键共价连接到 DNA 合成抑制剂米托蒽醌上。我们假设 Con-3 和 Con-7 与 OCC 的 GnRH-R 结合会将共轭的米托蒽醌暴露于细胞硫氧还蛋白,从而还原 Con-3 和 Con-7 的二硫键。随后释放的米托蒽醌导致其细胞内积累,从而发挥其细胞毒性作用。为了验证这一假设,我们使用 SKOV-3 人 OCC 确定了 Con-3 和 Con-7 的细胞毒性作用。Con-3 和 Con-7 的处理,但不是它们未共轭的 GnRH 对应物,导致米托蒽醌在 SKOV-3 细胞内积累,增加其凋亡,并减少其增殖,呈剂量和时间依赖性,半最大抑制浓度为 0.6-0.9 µM。结论是 Con-3 和 Con-7 作为细胞毒性“前药”起作用,其中米托蒽醌以 GnRH-R 特异性方式递送,并构成用于靶向卵巢肿瘤的新型抗癌药物的先导化合物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea45/11397358/3c2cf8f711a6/molecules-29-04127-g001.jpg

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