Project description:RNAseq files for Mullighan BiTE RNASEQ1 paper titled "Tumor intrinsic and extrinsic mechanisms of response and resistance to blinatumomab in relapsed/refractory acute lymphoblastic leukemia"
Project description:lowinput RNASEQ files for Mullighan BiTE RNASEQ2 paper titled "Tumor intrinsic and extrinsic mechanisms of response and resistance to blinatumomab in relapsed/refractory acute lymphoblastic leukemia"
Project description:The myocyte enhancer factor 2 (MEF2) gene family plays fundamental roles in the genetic programs that control cell differentiation, morphogenesis, proliferation, and survival in a wide range of cell types. The molecular programs they regulate and their role in tumor development and progression remain incompletely understood. The present study evaluated whether the MEF2D transcription factor functions as a tumor suppressor in breast cancer. We found knockout of the MEF2D gene in mouse mammary epithelial cells resulted in phenotypic changes characteristic of neoplastic transformation, including: enhanced cell proliferation, loss of contact inhibition, and anchorage-independent growth in soft agar, as well as capacity for tumor development in mice. Through RNAseq analysis, we found knockout of MEF2D induced the epithelial-to-mesenchymal transition (EMT) and activated several oncogenic signaling pathways. In summary, our study indicates that MEF2D may be a putative tumor suppressor, acting through selective gene regulatory programs that have clinical and therapeutic significance in breast cancer.
Project description:Global expression profiles in Huh7 after infection with Lv-shMEF2D and Lv-scrambled, as well as transfection with siRNA-MEF2D and siRNA-control, were compared to investigate the molecular mechanisms involved in MEF2D-mediated regulation of cell cycle. In order to investigate the molecular mechanisms involved in MEF2D-mediated regulation of cell cycle, we assessed gene expression profiles in Huh7 cells after infection with Lv-shMEF2D and Lv-scrambled, as well as transfection with siRNA-MEF2D and siRNA-control, by cDNA microarray. Analysis of global mRNA expression profile indicated a shift toward G2/M arrest in the cells after downregulating MEF2D expression. The genes that inhibit G2/M transition were found to be expressed in high level in MEF2D-downregulated group, as compared with control group. Meanwhile, mRNA abundance of G2/M transition-promoting genes, except CDC2 and CDC25C, was reduced when MEF2D expression was depressed in Huh7 cells
Project description:To analyze the expression profile in the Mef2d KO retina, we performed a microarray analysis using wild-type and Mef2d KO retina at P14. We performed a microarray analysis using wild-type and Mef2d KO retina at P14, and compared the expression profiles.
Project description:To explore the mechanisms underlying the maintenance of acute lymphoblastic leukemia harboring fusion genes involving MEF2D transcription factor, the MEF2D-fusion was silenced by shRNA and the resulting gene expression changes were analyzed by RNA-seq.