Project description:RNA-seq analysis was performed using zebrafish primary tumors and control thymus to analyze gene expression changes after IRF4 overexpression.
Project description:H3K27ac ChIP-seq analysis was performed using zebrafish normal thymus and primary tumors to analyze potential regulatory elements activated by IRF4 overexpression.
Project description:Single cell RNA-seq analysis was carried out for 1 normal sample from a control zebrafish line (lck-mCherry) and 5 non-tumor and 14 tumor samples from the IRF4 transgenic line (lck-IRF4). Tumor cells were harvested from the animals with or without heterozygous p53 mutation at different time points of tumor development.
Project description:Zebrafish CNS-PNET tumors were generated by activating NRAS in oligoneural precursor cells. Gene expression in the zebrafish brain tumors and normal zebrafish brain was analyzed by RNA-seq.
Project description:Cutaneous melanoma (CM) and uveal melanoma (UM) both originate from the melanocytic lineage but are primarily driven by distinct oncogenic drivers, BRAF/NRAS or GNAQ/GNA11 respectively. The melanocytic master transcriptional regulator, MITF, is essential for both CM development and maintenance, but its role in UM is largely unexplored. Here, we use zebrafish models to dissect the key UM oncogenic signaling events, and establish the role of MITF in UM tumors. Remarkably, mitfa deficiency was profoundly UM promoting, dramatically accelerating the onset and progression of tumors induced by Tg(mitfa:GNAQQ209L);tp53M214K/M214K. To further explore the role of MITF in GNAQ-driven tumorigenesis, we performed phospho-proteomics and total proteomics on 5 zebrafish GNAQ Tg(mitfa:GNAQQ209L);tp53M214K/M214K tumors and 5 zebrafish GNAQ Tg(mitfa:GNAQQ209L);tp53M214K/M214K;mitfa-/- tumors.