A Molecular Portrait of the replication stress response defects via Genome-wide Transcriptome Profiling. Homo sapiens

Defects in replication stress response (RSR) allow the survival and proliferation of genomically unstable cells, ultimately leading to tumorigenesis. Therefore, the RSR status can potentially serve as a powerful indicator to predict the possibility of early tumorigenesis. Here, we identified an RSR defects (RSRD) gene signature that robustly predicted RSR status. For the clinical benefit, our identification of RSRD gene signature gives the possibility to assess the risk of early tumorigenesis in the precancerous patients. Overall design: Various shRNAs that target genes involved in replication stress response were transfected in MCF-10A non-transformed breast cell lines after oncogenic cyclin E overexpressed. All MCF-10A variants were seeded 200000 at 10 cm plate. Cells were harvested after 48 hours culturing and used for gene expression profiling.