Abstract

BackgroundRenal cell carcinoma (RCC), including pediatric RCC, is one of the high cancer-associated death cause in adults and children. The mechanism by which long non-coding RNA SCAMP1 regulates RCC is not fully understood. MethodsmRNA and protein levels were detected by RT-qPCR and westernblot. MTT assay was used to examine cell viability and TUNEL assay was utilized to measure apoptosis of ACHN and Caki-1 cells.in vivo tumor growth was determined by xenograft assay. ResultsH2O2 treatment remarkably inhibited RCC cell viability and induced apoptosis. SCAMP1 was elevated in RCC cells and tumors. SCAMP1 depletion attenuated cell viability and promoted apoptosis under H2O2 treatment. Then, miR-429 was identified as downstream effector for SCAMP1-mediated tumorigenesis under H2O2 treatment. Besides, miR-429 was downregulated in human clinical tumors. ZEB1 and JUN were both found to be involved in the role of miR-429 in RCC. More interestingly, autophagy obviously affected miR-429-modulated RCC tumorigenesis. Eventually, we also showed that SCAMP1 played an oncogenic role in vivo. ConclusionIn summary, we propose that SCAMP1 affects RCC tumorigenesis through miR-429 and its downstream targets. Our findings will contribute to development of biomarkers and therapeutics for RCC.

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