Ge Jiejie, Liu Meng, Zhang Yuchao, Xie Linsen, Shi Zhisong, Wang Guanghui
Department of Clinical Laboratory, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, China.
Department of Clinical Laboratory, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
J Biochem Mol Toxicol. 2022 Jun;36(6):e23031. doi: 10.1002/jbt.23031. Epub 2022 Mar 10.
LncRNAs have been suggested to participate in the growth and metastasis of cancer through a variety of molecular mechanisms. Recently, SNHG10, a newly discovered lncRNA, is reported to play a role of an oncogene in osteosarcoma (OS) genesis. Nonetheless, the mechanism underlying OS remains unclear. The present work found that SNHG10 expression increased within OS cells and tissues, while suppressing its expression decreased OS cell proliferation, migration, invasion, but increased their apoptosis. As for the mechanism, we confirmed that SNHG10 could bind to miR-141-3p, while the latter could bind to WTAP. SNHG10 upregulated WTAP through decreasing miR-141-3p expression. More importantly, SNHG10 deletion remarkably reduced proliferation, migration, and invasion of cells, but accelerated their apoptosis. However, when cells were subjected to miR-141-3p inhibitor cotransfection or overexpressed WTAP, these effects were partially recovered. In summary, this study suggested that the expression of SNHG10 markedly elevated within OS, and the SNHG10/miR-141-3p/WTAP axis facilitated OS progression.
已有研究表明，长链非编码RNA（lncRNAs）可通过多种分子机制参与癌症的生长和转移。最近，有报道称新发现的lncRNA SNHG10在骨肉瘤（OS）发生过程中发挥癌基因作用。然而，OS的潜在机制仍不清楚。目前的研究发现，SNHG10在OS细胞和组织中的表达增加，而抑制其表达则会降低OS细胞的增殖、迁移、侵袭能力，但会增加其凋亡。至于机制，我们证实SNHG10可以与miR-141-3p结合，而后者可以与WTAP结合。SNHG10通过降低miR-141-3p的表达上调WTAP。更重要的是，SNHG10缺失显著降低了细胞的增殖、迁移和侵袭能力，但加速了它们的凋亡。然而，当细胞共转染miR-141-3p抑制剂或过表达WTAP时，这些效应部分得到恢复。总之，本研究表明SNHG10在OS中的表达显著升高，且SNHG10/miR-141-3p/WTAP轴促进了OS的进展。
