| INTRODUC TI ONRenal cell carcinoma (RCC) is a common cancer that accounts for 2%-3% of all cancerous diseases in adults. 1 There are approximately 65 000 cases of RCC each year, and RCC is the eighth most common cause of cancer mortality. 2 RCC affects quality of life and life expectancy and has important health and economic implications related to metabolic syndromes, increased cardiovascular risk and end-stage kidney disease. 3 In addition, clear cell renal cell carcinoma (ccRCC) is the most universal subtype of RCC, accounting for approximately 75% of RCC. Furthermore, the morbidity and mortality rates of RCC are rising globally. 4 Besides traditional surgery, RCC is resistant to the other forms of therapies chemotherapy and radiotherapy. The 5-year survival rate of RCC is approximately 55%, while the 5-year survival rate of metastatic RCC is approximately 10%. 5 Patients with metastatic RCC are faced with a depressing prognosis and limited therapeutic options. The median survival time in a recent cohort study was only 1.5 years, and the survival rate was less than 10% in patients who survived 5 years. 6 Thus, it is vital to study the molecular basis of RCC to design novel therapeutic drugs to improve survival rates.Abstract Objective: We aimed to investigate the roles of the lncRNA MALAT1 in renal cell carcinoma (RCC) progression. Methods: qRT-PCR was used for the assessment of BIRC5, miRNA-203 and MALAT1 expression. Furthermore, the targeted relationships between miR-203 and BIRC5, as well as MALAT1 and miR-203, were predicted by the miRanda/starBase database and verified by dual-luciferase reporter gene assay. The effects of MALAT1, miRNA-203 and BIRC5 on cell proliferation, cell cycle, cell apoptosis, cell invasion and cell migration were studied by using CCK-8, flow cytometry, transwell and wound healing assays, respectively. In addition, the effects of MALAT1 on RCC tumorigenesis were evaluated in vivo by nude mouse tumorigenesis. Results: The expression levels of BIRC5 and MALAT1 were higher in RCC tissues and cell lines than in adjacent normal tissues and a normal renal cortex proximal tubule epithelial cell line. In contrast, the expression of miRNA-203 in RCC tissues and cell lines was higher than that in adjacent normal tissues and a normal renal cortex proximal tubule epithelial cell line. BIRC5 and MALAT1 promoted cell proliferation yet decreased the percentage of RCC cells at G0/G1 phase.
Conclusions:Our study demonstrated that MALAT1 functions as a miR-203 decoy to increase BIRC5 expression in RCC.