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.
Highlights
Chondrosarcoma is the second most common type of primary bone tumors and is derived from cartilageproducing cells[1]
In the present study, we for the first time found that SP1 induced the upregulation of small nucleolar RNA host gene 6 (SNHG6), which led to the suppression of KLF6 by recruiting EZH2 and promoted the tumorigenesis of chondrosarcoma
This novel mechanism is the first report about the function of SNHG6 in chondrosarcoma and revealed that long non-coding RNA (lncRNA) SNHG6 and KLF6 played an essential role during the progression of chondrosarcoma (Fig. S3)
Summary
Chondrosarcoma is the second most common type of primary bone tumors and is derived from cartilageproducing cells[1]. Cancer statistic data shows that the 10-year survival rate of patient with conventional chondrosarcoma in grade I, II, and III was 83, 64, and 29%, respectively[1]. Long non-coding RA (lncRNA) is one family of noncoding RNAs with >200 nucleotides in length that have versatile functions in numerous biological processes, including tumor progression and inhibition[3]. Xing Bao and his colleagues found that lncRNA HOTAIR was upregulated in chondrosarcoma tissues and showed positive correlation with the tumor stage and poor prognosis, while knockdown of HOTAIR inhibited the growth of chondrosarcoma cells in vitro and in vivo[4].
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