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钌配合物 HB324 通过上调 Harakiri 诱导神经母细胞瘤细胞凋亡并克服顺铂耐药性。

Ruthenium Complex HB324 Induces Apoptosis via Mitochondrial Pathway with an Upregulation of Harakiri and Overcomes Cisplatin Resistance in Neuroblastoma Cells In Vitro.

机构信息

Department of Pediatric Oncology/Hematology, Helios Clinics Schwerin, Wismarsche Straße 393-397, 19049 Schwerin, Germany.

Medical School Hamburg (MSH), University of Applied Sciences and Medical University, Am Kaiserkai 1, 20457 Hamburg, Germany.

出版信息

Int J Mol Sci. 2023 Jan 4;24(2):952. doi: 10.3390/ijms24020952.

Abstract

Ruthenium(II) complexes with N-heterocyclic carbene (NHC) ligands have recently attracted attention as novel chemotherapeutic agents. The complex HB324 was intensively studied as an apoptosis-inducing compound in resistant cell lines. HB324 induced apoptosis via mitochondrial pathways. Of particular interest is the upregulation of the Harakiri resistance protein, which inhibits the anti-apoptotic and death repressor proteins Bcl-2 (B-cell lymphoma 2) and BCL-xL (B-cell lymphoma-extra large). Moreover, HB324 showed synergistic activity with various established anticancer drugs and overcame resistance in several cell lines, such as neuroblastoma cells. In conclusion, HB324 showed promising potential as a novel anticancer agent in vitro, suggesting further investigations on this and other preclinical ruthenium drug candidates.

摘要

钌(II)配合物与 N-杂环卡宾(NHC)配体作为新型化疗药物引起了人们的关注。HB324 复合物作为一种诱导凋亡的化合物在耐药细胞系中得到了深入研究。HB324 通过线粒体途径诱导细胞凋亡。特别值得注意的是,上调了 Harakiri 抗性蛋白,该蛋白抑制了抗凋亡和死亡抑制蛋白 Bcl-2(B 细胞淋巴瘤 2)和 BCL-xL(B 细胞淋巴瘤-特大)。此外,HB324 与各种已建立的抗癌药物具有协同作用,并克服了几种细胞系中的耐药性,如神经母细胞瘤细胞。总之,HB324 在体外显示出作为新型抗癌药物的有前景的潜力,这表明需要对该药物和其他临床前钌候选药物进行进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f6e/9866957/c6566e3f2c07/ijms-24-00952-g001.jpg

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