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Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1‐like kinase‐1 expression by competitively binding microRNA‐125b and interacting with Snail1/2 in bladder cancer
Author(s) -
Wang Chunyang,
Tao Weiyang,
Ni Shaobin,
Chen Qiyin
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27387
Subject(s) - gene knockdown , downregulation and upregulation , small nucleolar rna , biology , cancer research , microrna , kinase , cell migration , cell growth , gene , long non coding rna , cell , western blot , cell culture , epithelial–mesenchymal transition , microbiology and biotechnology , genetics
Backgrounds/aims Numerous studies have reported that long noncoding RNAs (lncRNAs) play critical roles in the development and progression of bladder cancer (BC). LncRNA snoRNA host gene 6 (SNHG6) is ectopically expressed in tumor tissues of patients with BC and BC cell lines. However, little is known about the molecular mechanism of SNHG6‐mediated bladder urothelial carcinoma cell migration and invasion. Methods We detected the SNHG6 levels in human BC specimens and cell lines by quantitative real‐time polymerase chain reaction and Western blot, and investigated its role in BC using in vitro assays. Results We showed that overexpression of SNHG6 induced epithelial‐mesenchymal transition (EMT) and promoted the migration and invasion capabilities of BC cells. Mechanistically, SNHG6 induced EMT of BC cells by upregulating the expression levels of Snail1/2 and regulated BC cell migration and invasion by tumor suppressive hsa‐miR‐125b and its target gene NUAK Family Kinase 1 (NUAK1). Furthermore, we found that SNHG6 was positively correlated with Snail1/2 expression, and negatively correlated with hsa‐miR‐125b expression in BC specimens. Further study showed that SNHG6 repressed hsa‐miR‐125b expression to upregulate Snail1/2. Conversely, hsa‐miR‐125b knockdown augmented SNHG6 expression in BC cells. Conclusion Overall, our study demonstrated that SNHG6 promotes BC cell migration and invasion partly via the hsa‐miR‐125b/Snail1/2/NUAK1 pathway. Therefore, SNHG6 may be a potential prognostic biomarker in BC, and targeting hsa‐miR‐125b/Snail1/2/NUAK1 axis may be a promising therapeutic approach for BC patients.