1 Luoyang Orthopedic Hospital of Henan Province, Orthopedic Hospital of Henan Province, Henan, China.
2 Department of Orthopedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
DNA Cell Biol. 2019 Feb;38(2):170-175. doi: 10.1089/dna.2018.4424.
Long noncoding RNA host gene 16 (SNHG16) has a key role in a variety of cancer progression. However, the role and mechanism of SNHG16 in osteosarcoma (OS) remain unknown. In this study, we examined the functional role of SNHG16 in OS cells through knocked-down SNHG16 by using siRNA. We found that SNHG16 is overexpressed in OS tissues and cell lines. Inhibition of SNHG16 reduced OS cells proliferation, stimulated apoptosis, and decreased migration and invasion. In addition, SNHG16 reduced miR-340 expression in OS cells. The results showed that SNHG16 involves in the migration and invasion of OS cells through sponging miRNA-340. Together, our data support an important role of SNHG16 in regulating OS cell invasion and migration that highlights SNHG16 may be regarded as a potential target for OS treatment.
长链非编码 RNA 宿主基因 16（SNHG16）在多种癌症的进展中具有关键作用。然而，SNHG16 在骨肉瘤（OS）中的作用和机制尚不清楚。在这项研究中，我们通过使用 siRNA 敲低 SNHG16 来研究 SNHG16 在 OS 细胞中的功能作用。我们发现 SNHG16 在 OS 组织和细胞系中过表达。抑制 SNHG16 可降低 OS 细胞的增殖，刺激细胞凋亡，并减少迁移和侵袭。此外，SNHG16 降低了 OS 细胞中 miR-340 的表达。结果表明，SNHG16 通过海绵吸附 miRNA-340 参与 OS 细胞的迁移和侵袭。总之，我们的数据支持 SNHG16 在调节 OS 细胞侵袭和迁移中的重要作用，这表明 SNHG16 可能被视为 OS 治疗的潜在靶点。
