Genes regulated by JAK1/2 inhibitor ruxolitinib and myxoid liposarcoma-specific fusion onccogene FUS-DDIT3 in HT1080 cells.

Sarcomas and leukemias that are characterized by FET (FUS, EWSR1, TAF15) fusion oncogenes consist of more than 20 entities. Myxoid liposarcoma, one of the most common FET sarcoma types, is defined by the FUS-DDIT3 or the less common EWSR1-DDIT3 fusion oncogene. Previously, JAK-STAT signaling have been connected to cancer stem cell properties and chemotherapy resistance in myxoid liposarcoma, but the role of FUS-DDIT3 is not known. Therefore, we treated HT1080 fibrosarcoma cells expression FUS-DDIT3 with JAK1/2 inhibitor ruxolitinib and performed RNA sequencing of treated and control cells. Additionally, we analyzed native HT1080 cells to be able to compare the induced gene expression changes due to FUS-DDIT3 expression with those induced by JAK-STAT pathway inhibition. Overall design: RNA sequencing was performed on HT1080 fibrosarcoma cells expressing FUS-DDIT3-EGFP, treated with JAK 1/2 inhibitor ruxolitinib and untreated controls (n=3-4). For comparison, native HT1080 cells (n = 4) were included.