Chromatin states and transcription factor binding in SIX1 deficient Rhabdomyosarcoma cells

Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. To elucidate the mechanism by which SIX1 loss activates a differentiation program, we performed SIX1, MYOD1, and H3K27ac ChIPseq in two SIX1 knockdown SMS-CTR cell lines and one control SMS-CTR cell line to profile changes in transcriptional activity and myogenic transcription factor binding in fusion-negative Rhabdomyosarcoma. ChIPseq was performed to characterize genome-wide SIX1 and MYOD1 binding as well as H3K27ac deposition in Fusion-Negative Rhabdomyosarcoma cells (SMS-CTR). Two SIX1 knockdown SMS-CTR cell lines (SMS-CTR SIX1 KD5, SMS-CTR SIX1 KD6) and one control SMS-CTR cell line (SMS-CTR SCRAMBLE) were used.