LncRNA SNHG1 promotes renal cell carcinoma progression through regulation of HMGA2 via sponging miR‐103a

Background Long noncoding RNAs (LncRNAs) plays a vital role in tumorigenesis and development. The molecular mechanism of SNHG1 in renal cell carcinoma (RCC) has not been illustrated. The aim of this research was to explore the expression and function of LncRNA SNHG1 in RCC. Material and Methods The expression of SNHG1 in clinical tissues and RCC cell lines was detected. Luciferase reporter assay was performed to verify the correlation between SNHG1, miR‐103a, and HMGA2. CCK‐8 assay was performed to examine cell viability. Cell apoptosis was analyzed using flow cytometry. Cell invasion capacity was determined by Transwell assays. The protein level of HMGA2 was analyzed by Western blotting. Results The expression of SNHG1 markedly increased in RCC tissues and cell lines. Subsequent studies identified SNHG1 as a miRNA sponge for miR‐103a. In addition, SNHG1 knockdown and miR‐103a overexpression significantly inhibited progression of RCC. miR‐103a also regulated HMGA2 levels. Conclusion Our findings showed that SNHG1 was upregulated in RCC cells and tissues. SNHG1 promoted the malignant characteristics of RCC cells. Its regulatory effect may be regulation of HMGA2 by sponging miR‐103a. Therefore, Our study facilitates the understanding of SNHG1 function in RCC. SNHG1 exerted its oncogenic effect through modulating HMGA2 expression and acts as a ceRNA by sponging miR‐103a.