| Literature DB >> 33431838 |
Fei-Fei Pu1, De-Yao Shi1, Ting Chen1, Yu-Xuan Liu2, Bin-Long Zhong1, Zhi-Cai Zhang1, Wei-Jian Liu1, Qiang Wu1, Bai-Chuan Wang1, Zeng-Wu Shao1, Tong-Chuan He3, Jian-Xiang Liu4.
Abstract
Small nucleolar RNA host gene 6 (SNHG6) is a newly discovered long non-coding RNA (lncRNA), while the regulatory mechanism of SNHG6 in chondrosarcoma is largely unknown. Here we found that SNHG6 expression was upregulated and showed positive correlation with the progression of chondrosarcoma. Functional assays demonstrated that SNHG6 was required for the proliferation, migration, and invasion of chondrosarcoma cells. Mechanistic study revealed that SNHG6 could recruit EZH2 and maintain high level of H3K27me3 to repress the transcription of tumor-suppressor genes, including KLF6. KLF6 was found to bind to the promoter region of SP1 and restrained its transcription, while SP1 could be recruited to the promoter region of SNHG6 and promoted its transcription to form a positive loop. In summary, this study reveals that SP1-induced SNHG6 forms a positive loop to facilitate the carcinogenesis of chondrosarcoma through the suppression of KLF6 by recruiting EZH2, which manifests the oncogenic function of SNHG6 in chondrosarcoma.Entities:
Year: 2021 PMID: 33431838 PMCID: PMC7801621 DOI: 10.1038/s41419-020-03352-6
Source DB: PubMed Journal: Cell Death Dis Impact factor: 8.469