Inhibition of chaetocin on retinoblastoma progression by modulating the miR-124/SBK1 axis

IF 0.7 4区 材料科学 Q3 Materials Science Materials Express Pub Date : 2023-12-01 DOI:10.1166/mex.2023.2510
Qiaoling Sun, Xiaozhao Zhao, Bei Jin, Baotong Shu, Yu Ma
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Abstract

We conducted cellular and animal experiments to investigate the correlation between miR-124/SBK1 and retinoblastoma (RB) progression, as well as to elucidate the anti-cancer efficacy of chaetocin in RB. Initially, miR-124 levels showed a significant decrease in RB tissues and cells, which further declined with increasing tumor diameter and clinical stage. In cellular experiments, inhibiting miR-124 expression significantly enhanced the viability and invasiveness of Y79 cells, while up-regulating miR-124 suppressed the malignant biology of Y79 cells by targeting SBK1 levels, thereby reducing their viability and invasiveness. Subsequent animal experiments provided further evidence that SBK1 was the functional target of miR-124, and its up-regulation significantly facilitated RB progression. Additionally, chaetocin demonstrated anti-tumor effects through the upregulation of miR-124 and downregulation of SBK1. Therefore, chaetocin can effectively inhibit RB progression by targeting the upregulation of miR-124 and downregulation of SBK1.
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通过调节 miR-124/SBK1 轴抑制视网膜母细胞瘤的发展
我们通过细胞和动物实验研究miR-124/SBK1与视网膜母细胞瘤(retinoblastoma, RB)进展的相关性,并阐明缩宫素对RB的抗癌作用。最初,miR-124水平在RB组织和细胞中显著降低,随着肿瘤直径和临床分期的增加,miR-124水平进一步下降。在细胞实验中,抑制miR-124的表达可显著增强Y79细胞的活力和侵袭性,而上调miR-124可通过靶向SBK1水平抑制Y79细胞的恶性生物学,从而降低其活力和侵袭性。随后的动物实验进一步证明,SBK1是miR-124的功能靶点,其上调可显著促进RB的进展。此外,催产素通过上调miR-124和下调SBK1显示出抗肿瘤作用。因此,催产素可以通过靶向miR-124的上调和SBK1的下调,有效抑制RB进展。
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Materials Express
Materials Express NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
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>12 weeks
期刊介绍: Information not localized
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