Effect of Jab1 knockdown on gene expression during disease progression in acute myeloid leukemia
The progression of acute myeloid leukemia (AML) is a complex process involving various cellular activities. In this context, our research focuses on the role of Jab1 as a key regulatory factor. Specifically, Jab1 plays a crucial role in regulating apoptosis and proliferation, providing support for the proliferation and survival of AML cells. As a c-JUN transcription co-activator, Jab1 participates in multiple transcriptional regulatory networks, influencing the gene expression of cells. Through RNA-seq data analysis, we present a detailed molecular framework, elucidating the impact of Jab1 downregulation on gene expression. This provides important insights for a comprehensive understanding of the molecular mechanisms underlying this disease, offering robust support for future research and therapeutic strategies. Overall design: To investigate the regulatory role of Jab1 in the proliferation and survival of acute myeloid leukemia cells, we established a cell line using shRNA to knock down the target gene in MOLM13 cells.