Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
General Medicine, Ningxia Hui Autonomous Region People's Hospital, Yinchuan, Ningxia, China.
J Cell Biochem. 2020 Oct;121(10):4034-4042. doi: 10.1002/jcb.29569. Epub 2020 Jan 21.
Thyroid cancer (TC) has been characterized as the most common malignant malady of the endocrine system. Small nucleolar RNA host gene 7 (SNHG7) has been reported to serve as a key regulator in a large number of human cancer types, but its role in TC and the underlying regulatory mechanism have never been evaluated yet. The present study indicated that the expression of SNHG7 was markedly higher in TC cell lines. Knockdown of SNHG7 led to a suppression of TC cell progression and migration. Acyl-CoA synthetase long-chain family member 1 (ACSL1) has also been demonstrated as an oncogene in many cancers. Herein an inhibition of ACSL1 after SNHG7 knockdown was captured. Further, the suppressing effects of SNHG7 knockdown on TC cell processes were counteracted by ACSL1 overexpression. Data from online bioinformatics analysis, RNA immunoprecipitation, and luciferase reporter assays validated the interaction between microRNA-449a (miR-449a) and SNHG7 or ACSL1. It was also verified that SNHG7 sequestered miR-449a and therefore elevated ACSL1 expression levels. To conclude, the current study indicated that SNHG7 promoted proliferation and migration of TC cells by sponging miR-449a and therefore upregulating ACSL1. The present study may provide more explorations about the molecular regulation mechanism of long noncoding RNAs in TC progression.
甲状腺癌（TC）已被描述为内分泌系统最常见的恶性疾病。小核仁 RNA 宿主基因 7（SNHG7）已被报道在许多人类癌症类型中作为关键调节剂发挥作用，但它在 TC 中的作用及其潜在的调节机制尚未得到评估。本研究表明，SNHG7 在 TC 细胞系中的表达明显升高。SNHG7 的敲低导致 TC 细胞的进展和迁移受到抑制。酰基辅酶 A 合成酶长链家族成员 1（ACSL1）也已被证明是许多癌症中的癌基因。在此，我们发现 SNHG7 敲低后 ACSL1 的表达受到抑制。进一步的，ACSL1 的过表达逆转了 SNHG7 敲低对 TC 细胞过程的抑制作用。在线生物信息学分析、RNA 免疫沉淀和荧光素酶报告基因分析的数据验证了 microRNA-449a（miR-449a）与 SNHG7 或 ACSL1 之间的相互作用。还验证了 SNHG7 可以结合 miR-449a，从而提高 ACSL1 的表达水平。总之，本研究表明，SNHG7 通过海绵吸附 miR-449a 促进 TC 细胞的增殖和迁移，从而上调 ACSL1。本研究可能为长链非编码 RNA 在 TC 进展中的分子调控机制提供更多的探索。
