Abstract:
:The present study aimed to investigate the expression of microRNA (miRNA or miR)-186 in tumor tissue, blood and urine from patients with bladder cancer. The mechanism by which miR-186 regulates the invasion and metastasis of bladder cancer was also assessed. A total of 76 patients who underwent surgical resection of bladder cancer tissues between August 2012 and January 2016 were included in the present study. Blood and urine samples were also collected from the 76 patients and another 66 healthy subjects. Expression of vascular endothelial growth factor C (VEGF-C) mRNA and miR-186 was measured using reverse transcription-quantitative polymerase chain reaction. Western blot analysis was performed to assess VEGF-C protein expression in tumor tissues. The content of VEGF-C protein in blood and urine samples was measured using an enzyme-linked immunosorbent assay. To identify the direct interaction between miR-186 and VEGF-C mRNA, a dual luciferase reporter assay was performed. The present findings demonstrated that VEGF-C mRNA expression in tumor tissues, blood and urine of bladder cancer patients was upregulated. VEGF-C protein expression in bladder cancer tissues was also enhanced. VEGF-C protein content in blood and urine from bladder cancer patients was elevated, consistent with the results for VEGF-C mRNA. Expression of miR-186 was reduced in tumor tissues, blood and urine. Dual luciferase reporter assay demonstrated that miR-186 regulated the expression of VEGF-C by binding with its 3'-untranslated region. Therefore, the results of the present study indicate that the expression of VEGF-C mRNA and protein is upregulated in tumor tissues, blood and urine from patients with bladder cancer, while that of miR-186 is downregulated in these samples. miR-186 potentially regulates the invasion and metastasis of bladder cancer via VEGF-C, and may become a gene marker for bladder cancer in the future.
journal_name
Exp Ther Medjournal_title
Experimental and therapeutic medicineauthors
He X,Ping J,Wen Ddoi
10.3892/etm.2017.4908subject
Has Abstractpub_date
2017-10-01 00:00:00pages
3253-3258issue
4eissn
1792-0981issn
1792-1015pii
ETM-0-0-4908journal_volume
14pub_type
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