Up-regulation of SNHG16 induced by CTCF accelerates cardiac hypertrophy by targeting miR-182-5p/IGF1 axis.

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.