Gene expression profiling of HCCLM3 cells: Control ASO vs SCARNA13 ASO

Understanding the roles of ncRNAs in tumorigenesis and metastasis would establish avenues for the identification of diagnostic and therapeutic targets. We observed that lncRNA SNHG10 and its derived SCARNA13 were concomitantly upregulated in hepatocellular carcinoma (HCC) pulmonary metastases and associated with poor prognosis. Mechanistically, SCARNA13, modulated by SNHG10, facilitated the cell cycle and epithelial-mesenchymal transition (EMT) of HCC cells by promoting SOX9. SNHG10 served as a sponge for miR-150-5p and interacted with RPL4 mRNA to increase the expression and activity of c-Myb. Reciprocally, upregulated and hyperactivated c-Myb enhanced SNHG10 and SCARNA13 expression through regulating SNHG10 promoter activity, forming a positive feedback loop and continuously stimulating SCARNA13 expression. Our findings characterized a complex epigenetic cause of HCC with clinical implications. Overall design: To identify candidate downstream factors of SCARNA13, RNA-seq analysis was implemented for HCCLM3 cells with or without SCARNA13 knockdown.