Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 121, Issue 2, Pages 1880-1889Publisher
WILEY
DOI: 10.1002/jcb.29423
Keywords
meningioma; miR-556-5p; SNHG1; TCF12; Wnt signaling pathway
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Funding
- Anhui colleges and universities natural science research project (Key project) [KJ2018A0812]
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Meningioma, as a sort of the malignantly intracranial tumors, has captured public attention for its second-highest morbidity all over the world. Long noncoding RNAs (lncRNAs), including lncRNA SNHG1, have been well known as essential players in the development of diverse cancers. However, the biological effect and regulatory mechanism of SNHG1 have not been mentioned in meningioma. In this work, it was discovered that SNHG1 was overexpressed in meningioma cell lines. SNHG1 deficiency restrained cell growth as well as accelerated apoptosis. Then mechanism experiments demonstrated that SNHG1 functioned as the role of sponging miR-556-5p and negatively regulated miR-556-5p expression. Moreover, it was verified that TCF12 is the direct downstream target of miR-556-5p. Furthermore, SNHG1/miR-556-5p/TCF12 axis promoted cell proliferation and suppressed cell apoptosis in meningioma via activating the Wnt signaling pathway. In the end, it was confirmed that TCF12 expression was positively regulated by SNHG1, and TCF12 could promote transcription of SNHG1 through binding with the promoter region of SNHG1. In conclusion, the SNHG1/miR-556-5p/TCF12 feedback loop promotes the tumorigenesis of meningioma through the Wnt signaling pathway.
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