MiR-335 suppresses cell proliferation and migration by upregulating CRKL in bladder cancer

X.-K. Liu, D. Chen, X. Li

Department of Urology, Wuhan Asia General Hospital, Wuhan, China. drxinli@yahoo.com

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• Oncology

OBJECTIVE: microRNAs (miRNAs) abnormal expression was proved to regulate the bladder cancer (BC) development. Here, we aimed to investigate the role of miR-335 played in BC.

MATERIALS AND METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot were used to examine the miR-335 and CRKL (CT10 regulator of kinase-like protein) expression level in BC. Methyl thiazolyl tetrazolium (MTT) and RT-qPCR were used to examine cell viability of BC cells. Cell transwell assay was used to assess the migratory ability of BC cells. The direct target of miR-335 in BC was verified by luciferase reporter assay.

RESULTS: The results showed that the expression of miR-335 and CRKL in normal and adjacent tissues showed no significant differences. Whereas, miR-335 expression in BC was significantly lower and CRKL expression was observably higher than normal. CRKL was verified as a specific target of miR-335 in BC cells and the relationship between CRKL and miR-335 expression was negatively correlated in BC tissues. Furthermore, CRKL siRNA group in BC cells remarkably inhibited cell proliferation and migration. MiR-335 mimic in BC cells remarkably curbed cell proliferation and migration and CRKL could reverse the proliferative and migratory ability of BC cells regulated by miR-335.

CONCLUSIONS: miR-335 could suppress BC cell proliferation and migration by upregulating of CRKL.

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