SRA

Ovarian cancer is an aggressive malignancy characterized by the ascitic fluid and peritoneal metastases. Cancer cells detach from the extracellular matrix and survives the loss of anchorage in the ascites to disseminate extensively in the peritoneal cavity. Metabolic reprogramming is often observed in the cancer progression, yet its role in peritoneal metastasis is largely unexplored. Here we report that spermidine/spermine N1-acetyltransferase 1 (SAT1) promotes the anchorage-independent cell survival and potentiates metastatic dissemination. We compared the detached vs attached cells with RNAseq and identified that hypoxia was among the most enriched pathways using gene set enrichment analysis.To define the underlying mechanism, we first carried out RNA-seq analysis of the detached ovarian cancer cells with or without knocking down SAT1 and identified 1,829 differentially expressed genes (P?value?<?0.05) in the detached SAT1 knocking down cells. Gene Ontology (GO) term enrichment analysis recognized the differentially expressed genes associated extensively with mitotic process, most likely reflecting a role of SAT1 in cell cycle control. Taken together, our data suggest that SAT1 was induced by hypoxia in the detached cell and played an important role in cell cycle control. Overall design: To investigate effect of detachment culture condition and depletion of SAT1 on gene expression, we knocked down SAT1 in ovarian cancer cell line SKOV3 in attached and detached conditions by shRNA. We then perfromedcomparative gene expression profiling analysis of RNA-seq data for SKOV3 control cells (pLKO) in both detached and attached conditions and its SAT1 knockdown derivative (shSAT1) in detached condition.