Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing 400016, China.
Qinggang Senior Care Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Aging (Albany NY). 2021 Dec 13;13(23):25138-25152. doi: 10.18632/aging.203732.
The long non-coding RNA (lncRNA) SNHG3 has been shown to play oncogenic roles in several cancer types, but the mechanisms underlying its activity are poorly understood. In this study, we aimed to explore the clinical relevance and mechanistic role of SNHG3 in gastric cancer (GC). We found that SNHG3 expression in GC cell lines and tissues was significantly increased, and the upregulation of this lncRNA was correlated with tumor clinical stage and decreased patient survival. Knocking down SNHG3 in GC cells impaired the proliferative, migratory, and invasive activity and constrained GC xenograft tumor growth. Mechanistically, SNHG3 was found to bind and sequester miR-139-5p, thereby indirectly promoting the upregulation of the miR-139-5p target gene MYB. These data demonstrated that SNHG3 functions in an oncogenic manner to drive GC proliferation, migration, and invasion by regulating the miR-139-5p/MYB axis.
长链非编码 RNA(lncRNA)SNHG3 在多种癌症类型中表现出致癌作用,但其活性的机制尚不清楚。在这项研究中,我们旨在探讨 SNHG3 在胃癌(GC)中的临床相关性和机制作用。我们发现 SNHG3 在 GC 细胞系和组织中的表达显著增加,并且这种 lncRNA 的上调与肿瘤临床分期和患者生存时间缩短相关。在 GC 细胞中敲低 SNHG3 会削弱其增殖、迁移和侵袭活性,并抑制 GC 异种移植肿瘤的生长。从机制上讲,发现 SNHG3 可以结合并隔离 miR-139-5p,从而间接促进 miR-139-5p 靶基因 MYB 的上调。这些数据表明,SNHG3 通过调节 miR-139-5p/MYB 轴以致癌方式发挥作用,从而驱动 GC 的增殖、迁移和侵袭。