Project description:The activation of different oncogenic signals may primarily contribute to the heterogeneity of cancer cells. However, the exact mechanisms underlying different oncogenic transformation are still unclear. We used the c-Myc, H-Ras and Akt transformed liver cell model to define mRNA expression profiles in the non-transformed and the three types of oncogene-transformed cells Purified p53-/- mouse fetal liver progenitor cells were transformed by three oncogenic genetic factors, c-Myc, H-RasV12 and myristoylated-AKT1(myr-Akt). The gene expression profilings of transformed cells and control cells were analyzed through microarray.
Project description:The goal of this study is to develop a Plag1 signature and determine how its overexpression contributes to leukemogenesis. To study this, we transduced an immortalized (but not transformed) cell line (derived from Gata1s mutant fetal liver progenitor through insertional mutagenesis) by Plag1-expressing retrovirus. This turned a non-transformed cell line to a leukemogenic cell line. To study whether Plag1 overexpression led to deregulation of signaling pathways that may contribute to leukemic transformation, we generated microarray gene expression profiles of this cell line transduced with either Plag1 or the empty vector.
Project description:The activation of different oncogenic signals may primarily contribute to the heterogeneity of cancer cells. However, the exact mechanisms underlying different oncogenic transformation are still unclear. We used the c-Myc, H-Ras and Akt transformed liver cell model to define mRNA expression profiles in the non-transformed and the three types of oncogene-transformed cells
