Long non‐coding RNA (lncRNA) SNHG16 has been reported to be significant regulators in multiple cancers. However, never has the relationship between it and cardiac hypertrophy been studied until now. In this study, angiotensin II (Ang II)‐treated cardiomyocytes isolated from neonatal mice were used as a model of cardiac hypertrophy in vitro. Real‐time quantitative polymerase chain reaction was performed to measure the expression of SNHG16, miR‐182‐5p, and insulin‐like growth factor 1 (IGF1). The relationship between SNHG16 and its downstream genes were corroborated by RNA pull‐down and luciferase reporter experiments. Western blot was conducted to detect the expression of markers of hypertrophy. The results disclosed that SNHG16 expression was in a high level in the cardiac hypertrophic model. Down‐regulation of SNHG16 could decline the expression of hypertrophic markers and reduce cell surface area induced by Ang II. Moreover, SNHG16 was discovered to be activated by transcription factor CCCTC‐binding factor. In addition, SNHG16 could enlarge cell surface area and increase the expression of hypertrophic markers by inhibiting miR‐182‐5p expression in Ang II‐treated cardiomyocytes. Finally, overexpression of IGF1 could rescue the effects of silenced SNHG16 on cardiac hypertrophy cells. In brief, our study illustrated that silenced SNHG16 repressed Ang II‐imposed cardiac hypertrophy via targeting miR‐182‐5p/IGF1 axis.

中文翻译：

---

CTCF诱导的SNHG16的上调通过靶向miR-182-5p / IGF1轴来加速心脏肥大。

据报道，长非编码RNA（lncRNA）SNHG16是多种癌症中的重要调节剂。但是，迄今为止，尚未研究它与心脏肥大之间的关系。在这项研究中，将从新生小鼠体内分离的血管紧张素II（Ang II）处理的心肌细胞用作体外心肌肥大的模型。进行实时定量聚合酶链反应以测量SNHG16，miR-182-5p和胰岛素样生长因子1（IGF1）的表达。RNA下拉和荧光素酶报告基因实验证实了SNHG16及其下游基因之间的关系。进行蛋白质印迹以检测肥大标志物的表达。结果公开了在心脏肥大模型中SNHG16表达高水平。SNHG16的下调可能会降低肥大标志物的表达并减少Ang II诱导的细胞表面积。此外，发现SNHG16被转录因子CCCTC结合因子激活。此外，SNHG16可以通过抑制Ang II处理的心肌细胞中的miR‐182-5p表达来扩大细胞表面积并增加肥大标志物的表达。最后，IGF1的过表达可以挽救沉默的SNHG16对心肌肥大细胞的作用。简而言之，我们的研究表明，沉默的SNHG16通过靶向miR-182-5p / IGF1轴来抑制Ang II引起的心脏肥大。SNHG16可以通过抑制Ang II处理的心肌细胞中的miR‐182‐5p表达来扩大细胞表面积并增加肥大标志物的表达。最后，IGF1的过表达可以挽救沉默的SNHG16对心肌肥大细胞的作用。简而言之，我们的研究表明，沉默的SNHG16通过靶向miR-182-5p / IGF1轴抑制了Ang II引起的心脏肥大。SNHG16可以通过抑制Ang II处理的心肌细胞中的miR‐182‐5p表达来扩大细胞表面积并增加肥大标志物的表达。最后，IGF1的过表达可以挽救沉默的SNHG16对心肌肥大细胞的作用。简而言之，我们的研究表明，沉默的SNHG16通过靶向miR-182-5p / IGF1轴抑制了Ang II引起的心脏肥大。