LNCRNA SNHG7 PROMOTES TUMOR METASTASIS OF BLADDER CANCER BY INHIBITING MIR-34A

Cuiqing Shang^#, Jinyan Zhu^#, Chuanhua Zhang, Jingdong Yuan, Juan Yang, Qian Huang, YiPeng Liu^*

Department of Urology, The No.1 Hospital of Wuhan, Wuhan, 430000, China 

Objective: Long non-coding RNA(lncRNA) has become a key regulatory factor for tumor progression. lncRNA SNHG7 is considered to be a carcinogenic factor, but its role and mechanism in bladder cancer (BC) need to be further elaborated. To explore the role and mechanism of lncRNA SNHG7 in BC. 

Methods: PCR-qRT was used to detect the expression of SNHG7 and miR-34a in BC cells and normal cells. Stable and SNHG7 inhibitory vector and miR-34a over-expression vector were established and transfected into BC cells. CCK-8, traswell and flow cytometry were used to observe the proliferation and apoptosis of transfected cells. Western blot was used to detect the changes of EMT markers (E-cadherin, N-cadherin, Vimentin). The relationship between SNHG7 and miR-34a was determined using double luciferase report. 

Results: SNHG7 was up-regulated in BC cells, while miR-34a was down-regulated. Inhibition of SNHG7 or over-expression of miR-34a on cancer cells could inhibit the proliferation and invasion of cells and increase apoptosis rate. In addition, it could up-regulate E-cadherin and down-regulate N-cadherin and Vimentin. Double luciferase reported that SNHG7 and miR-34a could be targeted combined. Rescue experiments found that inhibition of miR-34a could reverse the biological function changes of cancer cells caused by inhibition of SNHG7.

Conclusion: SNHG7 can promote the proliferation, invasion, EMT and inhibit apoptosis of BC cells through miR-34a.