The purpose of our study was aimed to determine the functional role of microRNA (miR)-182 in clear cell renal cell carcinoma (ccRCC) and try to clarify its underlying molecular mechanism. Expression of miR-182 in both cancer and peripheral blood samples was analyzed by quantitative real-time PCR (qRT-PCR). Human RCC line Caki-1 cells were transfected with miR-182 mimic, miR-182 inhibitor, or negative controls, and then the cell viability, colony-formation ability, migration, and invasion assay were determined. Luciferase reporter assay, qRT-PCR and Western blotting were used to determine whether insulin-like growth factor 1 receptor (IGF1R) was a target of miR-182. Further, small interfering RNA (siRNA) against IGF1R was co-transfected with miR-182 inhibitor into cells, and then the effects on migration and invasion were assessed. MiR-182 was down-regulated in both cancer and blood samples compared to the matched non-tumor adjacent tissues and healthy volunteers, respectively (both P<0.05). Compared to the control group, cell viability, colony-forming ability, and numbers of migrated and invaded cells were significantly decreased by transfection with miR-182 mimic but were markedly increased by miR-182 inhibitor (all P < 0.05). Luciferase reporter assay confirmed that IGF1R was a target gene of miR-182, and IGF1R was negatively regulated by miR-182. Co-transfection of miR-182 inhibitor with si-IGF1R reversed the effect of miR-182 inhibitor on the migration and invasion of the cells. MiR-182 functions as an anti-oncogene in ccRCC, and miR-182-mediated inhibition of cell migration and invasion might be through directly targeting IGF1R. Key words: MicroRNA-182, clear cell renal cell carcinoma, migration and invasion, insulin-like growth factor 1 receptorRenal cell carcinoma (RCC) is the most common malignant tumor of adult kidney and accounts for approximately 3% of adult cancers with a high mortality at over 40% [1,2]. Clear cell renal cell carcinoma (ccRCC) is the most frequent subtype of RCC accounting for about 75-80% of the tumor [3]. Despite a tremendous advance has been made in available treatments, the prognosis still remains dismal for locally advanced and metastatic RCC [4]. It has been reported that up to 30-40% of patients with RCC present with metastatic disease even after radical resections [5]. Therefore, it is necessary to provide knowledge of molecule mechanisms controlling the metastatic and invasive potential of RCC.MicroRNAs (miRNAs) are a class of small and non-coding RNA molecules that regulate mRNA transcription and translation by base pairing with the 3' untranslated region (UTR) [6]. It has been well demonstrated that miRNAs are involved in the development and progression of various cancers by regulating cell proliferation, invasion, and migration [7,8]. Recently, emerging evidence has suggested the significant roles of miRNAs in RCC [9][10][11]. Among miRNAs, miR-182 was recently found to be associated with the invasive and/or metastatic potential of prostate cancer [12], melanoma [13], an...
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