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人参皂苷Rh7通过靶向ILF3-AS1介导的miR-212/SMAD1轴抑制非小细胞肺癌细胞的增殖、迁移和侵袭。

Ginsenoside Rh7 Suppresses Proliferation, Migration and Invasion of NSCLC Cells Through Targeting ILF3-AS1 Mediated miR-212/SMAD1 Axis.

作者信息

Chen Xiangbo, Liu Wenguang, Liu Bao

机构信息

Key Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, China.

出版信息

Front Oncol. 2021 Apr 29;11:656132. doi: 10.3389/fonc.2021.656132. eCollection 2021.

DOI:10.3389/fonc.2021.656132
PMID:33996578
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8116958/
Abstract

It is reported that ginsenosides have a significant anti-tumor effect on a variety of tumors. However, the role and mechanism of Rh7 in non-small cell lung cancer (NSCLC) are unclear. In this study, we aimed to study the anti-tumor effect of Rh7 on the proliferation and progression of NSCLC. Bioinformatics analysis showed that ILF3-AS1 was regulated by ginsenoside Rh7 in NSCLC. Down-regulation of ILF3-AS1 could significantly inhibit the proliferation, metastasis and invasion of NSCLC. In addition, ILF3-AS1 negatively controlled miR-212, which in turn targeted SMAD1 expression, thereby regulating NSCLC cell viability and apoptosis. Our results indicate that ILF3-AS1 can be used as a diagnostic and therapeutic target for non-small cell lung cancer. It is discovered for the first time that ginsenoside Rh7 inhibits the expression of ILF3-AS1 and exerts antitumor effects.

摘要

据报道,人参皂苷对多种肿瘤具有显著的抗肿瘤作用。然而,Rh7在非小细胞肺癌(NSCLC)中的作用及机制尚不清楚。在本研究中,我们旨在研究Rh7对NSCLC增殖和进展的抗肿瘤作用。生物信息学分析表明,在NSCLC中,ILF3-AS1受人参皂苷Rh7调控。ILF3-AS1的下调可显著抑制NSCLC的增殖、转移和侵袭。此外,ILF3-AS1负调控miR-212,而miR-212反过来靶向SMAD1的表达,从而调节NSCLC细胞的活力和凋亡。我们的结果表明,ILF3-AS1可作为非小细胞肺癌的诊断和治疗靶点。首次发现人参皂苷Rh7抑制ILF3-AS1的表达并发挥抗肿瘤作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec51/8116958/0ee7730e5c96/fonc-11-656132-g010.jpg
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