{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T03:36:24Z","timestamp":1771472184879,"version":"3.50.1"},"reference-count":34,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2020,5,3]],"date-time":"2020-05-03T00:00:00Z","timestamp":1588464000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biology International"],"published-print":{"date-parts":[[2020,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Long non\u2010coding 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)\u2010treated cardiomyocytes isolated from neonatal mice were used as a model of cardiac hypertrophy in vitro. Real\u2010time quantitative polymerase chain reaction was performed to measure the expression of SNHG16, miR\u2010182\u20105p, and insulin\u2010like growth factor 1 (IGF1). The relationship between SNHG16 and its downstream genes were corroborated by RNA pull\u2010down 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\u2010regulation 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\u2010binding factor. In addition, SNHG16 could enlarge cell surface area and increase the expression of hypertrophic markers by inhibiting miR\u2010182\u20105p expression in Ang II\u2010treated 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\u2010imposed cardiac hypertrophy via targeting miR\u2010182\u20105p\/IGF1 axis.<\/jats:p>","DOI":"10.1002\/cbin.11333","type":"journal-article","created":{"date-parts":[[2020,3,3]],"date-time":"2020-03-03T11:45:58Z","timestamp":1583235958000},"page":"1426-1435","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Up\u2010regulation of SNHG16 induced by CTCF accelerates cardiac hypertrophy by targeting miR\u2010182\u20105p\/IGF1 axis"],"prefix":"10.1002","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7598-4513","authenticated-orcid":false,"given":"Dong","family":"Wang","sequence":"first","affiliation":[{"name":"VIP Ward, Affiliated Hospital of Traditional Chinese Medicine Xinjiang Medical University  Urumqi 830000 Xinjiang 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