Preliminary results indicate increased expression of miR-184 in patients with renal carcinoma

J. Yang, C.-C. Lai, Z.-M. Xian, W.-Q. Wang, B.-L. Xu

Department of Clinical Laboratory, Maternity and Child-Care Hospital of Pingshan District (Maternity and Child-Care Hospital, Shenzhen University), Shenzhen, Guangdong, China. canbeiyan82@163.com

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• Oncology

OBJECTIVE: Renal carcinoma is the second most common cancer in the urinary system with an increasing trend. The major treatment for renal carcinoma is surgery, which results in unfavorable prognosis at times. As a tissue-specific marker for tumor, microRNA (miR) exerts its functions via facilitating oncogenic gene expression or suppressing tumor suppressor gene. MiR-184 is known to be abnormally expressed in various tumors. There are few studies about the lack of miR-184 expression in renal carcinoma.

PATIENTS AND METHODS: Real time-Polymerase Chain Reaction (PCR) was used to measure the expression of miR-184 in 38 renal carcinoma and adjacent tissues. The in vitro cultured renal carcinoma cell line ACHN was transfected with miR-184 mimic or inhibitor. The expression of miR-184 was measured by real time-PCR, and the cell proliferation was measured by MTT assay. The cell colony formation was examined, and the cell invasion potency was assessed by transwell assay. The apoptotic activity was measured by flow cytometry, and the Western blot detected protein expression change of β-catenin/TCF3 pathway.

RESULTS: Compared to tumor-adjacent tissues, miR-184 and β-catenin/TCF3 showed an elevated expression in renal carcinoma tissues which were further increased with elevated RC stages (p<0.05). The transfection of miR-184 mimic into ACHN cells increased its expression, enhanced ACHN cell proliferation, colony formation, inhibited apoptosis, promoted tumor cell invasion, and increased the expression of β-catenin and TCF4 proteins (p<0.05 compared to NC control group).

CONCLUSIONS: MiR-184 is up-regulated in renal carcinoma tissues. The downregulation of miR-184 in renal carcinoma cells could facilitate cell apoptosis and inhibited tumor proliferation or invasion possibly via modulating β-catenin/TCF4 pathway.

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