It is identified that long non-coding RNAs (lncRNAs) play important roles in
tumorigenesis.
LncRNA SNHG7 has been found to be an oncogene in varieties of
tumors including
bladder cancer. However, its potential regulatory mechanism in
bladder cancer still remains unknown. In this study, we discovered that the expression levels of SNHG7 were significantly increased in
bladder cancer tissues and cell lines. Patients with high expression level of SNHG7 suffered from poor prognosis. Additionally, knockdown of SNHG7 induced declined cell viability, proliferation as well as G0/G1 cell cycle arrest. Furthermore, we found that cell migratory ability was markedly reduced after silencing SNHG7. Next, we verified that knockdown of SNHG7 reduced the
protein level of β-
catenin and thus decreased the level of its downstream targets including c-myc,
cyclin D1 and
E-cadherin, implying that SNHG7 might impact
bladder cancer via Wnt/β-
catenin pathway. Subsequently, the rescue assays performed in SNHG7 silenced T24 cells by using activator of Wnt/β-
catenin signaling elucidated that re-activation of this pathway partly restored the inhibitory effects of SNHG7 suppression on
biological behaviors of T24 cells. Collectively, SNHG7 elicited carcinogenic functions in
bladder cancer partially via activating Wnt/β-
catenin signaling pathway, suggesting a potential target for the treatment and prognosis of
bladder cancer.