Growing evidence indicates that aberrant expression of microRNAs (miRNAs) contributes to tumorigenesis in various human malignancies. In this study we revealed that miR-195 acted as a tumor suppressor in renal cell carcinoma (RCC) through inhibition of HMGA1 expression. qRT-PCR was used to detect the miR-195 expression in RCC tissues and cell lines. RCC cell line Caki-1 and Caki-2 cells were used in this study. The luciferase report assay and rescue assay were performed to identify HMGA1 as the target gene of miR-195. Additionally, Kaplan-Meier method and log-rank test was used to explore the relationship between HMGA1 expression and RCC prognosis. We observed that miR-195 expression was significantly downregulated both in RCC tissues and in RCC cell lines. We observed that miR-195 overexpression inhibits the abilities of RCC cell proliferation, cell cycle progression and metastasis in vitro by targeting HMGA1 via epithelial to mesenchymal transition (EMT) pathway. In clinical specimens, HMGA1 was overexpressed in high-grade RCC when compared with its levels in normal tissues and low-grade RCC cancer, its expression levels were inversely correlated with overall survival. Our findings highlight an important role of miR-195 and HMGA1 in the molecular etiology of RCC, indicating that they can serve as potential biomarkers and therapy targets of RCC.
Keywords: HMGA1; RCC; metastasis; miR-195; proliferation.
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