Department of Biochemistry and Molecular Biology, School of Basic Medicine, Qingdao University, Qingdao, 266071, China.
Wanzhou District Center for Disease Control and Prevention, Chongqing, 404100, China.
Sci Rep. 2024 Feb 8;14(1):3265. doi: 10.1038/s41598-024-52953-0.
An increasing number of studies have indicated the crucial involvement of long non-coding RNAs (lncRNAs) in the onset and progression of malignancies. However, a complete understanding of the molecular mechanism underlying the effect of abnormally expressed lncRNAs on breast cancer (BC) remains elusive. This study aimed to elucidate the influence of the lncRNA small nucleolar RNA host gene 1 (SNHG1) on BC progression and its underlying mechanism. Our findings revealed a conspicuous up-regulation of SNHG1 in both BC tissues and cells. The downregulation of SNHG1 was observed to inhibit BC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) processes, while simultaneously promoting apoptosis. Furthermore, dual-luciferase reporter gene and RNA pull-down assays established that SNHG1 targeted miR-641 expression, while miR-641 targeted RRS1. Rescue studies demonstrated that in vitro SNHG1 silencing could be reversed by the miR-641 inhibitor, as well as by RRS1 upregulation. Moreover, in vivo downregulation of SNHG1 was found to inhibit BC growth. Through the inhibition of the miR-641 level, SNHG1 elevated the level of the downstream target RRS1, thereby fostering BC growth, migration, and invasion while inhibiting apoptosis. These findings suggest that SNHG1 may represent a potential therapeutic target for BC treatment.
越来越多的研究表明，长非编码 RNA（lncRNA）在恶性肿瘤的发生和发展中起着关键作用。然而，对于异常表达的 lncRNA 对乳腺癌（BC）影响的分子机制仍不完全清楚。本研究旨在阐明 lncRNA 小核仁 RNA 宿主基因 1（SNHG1）对 BC 进展的影响及其潜在机制。我们的研究结果表明，SNHG1 在 BC 组织和细胞中均明显上调。下调 SNHG1 可抑制 BC 细胞增殖、迁移、侵袭和上皮-间充质转化（EMT）过程，同时促进细胞凋亡。此外，双荧光素酶报告基因和 RNA 下拉实验证实 SNHG1 靶向 miR-641 的表达，而 miR-641 靶向 RRS1。挽救实验表明，miR-641 抑制剂和 RRS1 过表达均可逆转体外 SNHG1 沉默。此外，体内下调 SNHG1 可抑制 BC 生长。通过抑制 miR-641 水平，SNHG1 上调下游靶标 RRS1 的水平，从而促进 BC 的生长、迁移和侵袭，同时抑制细胞凋亡。这些发现表明，SNHG1 可能是治疗 BC 的潜在靶点。
