RNA-seq of TIF1 modulates the chromatin accessibility to regulate the self-renewal and differentiation of leukemic stem cells. Mus musculus

It is RNA-seq data of the project. Chronic myeloid leukemia (CML), characterized by expression of p210-BCR-ABL, is a clonal myeloproliferative disease initiated by malignant transformation of hematopoietic stem cells (HSC). Recently, high expression of TIF1b/TRIM28/KAP1 was correlated with poor prognosis in patients with various types of cancer, but the role of Tif1b in myeloid leukemia is unclear. To determine whether TIF1b promoted the development of BCR-ABL-induced myeloid leukemia in vivo, we generated BCR-ABL;Tif1bf/f;Cre-ERT2 compound mice by crossing Rosa26 locus BCR-ABL conditional knock-in mice and Tif1bf/f;Cre-ERT2 conditional KO mice. We transplanted BM cells isolated from Cre-ERT2 (WT), Tif1bf/f;Cre-ERT2 (Tif1b KO), BCR-ABL;Cre-ERT2 (BCR-ABL), and BCR-ABL;Tif1bf/f;Cre-ERT2 (BCR-ABL;Tif1b KO) mice into lethally irradiated CD45.1+ WT recipient mice, and injected tamoxifen 4 weeks after BM transplantation. To elucidate the mechanisms underlying the impaired development of leukemia in BCR-ABL;Tif1b KO mice, we performed NGS isolated from WT, Tif1b KO, BCR-ABL, BCR-ABL;Tif1b KO mice.