Transcriptomic profiling of AML cell lines MV4-11 and Kasumi-1 treated with CK1α degrader PinA1

Acute myeloid leukemia (AML) is characterized by dysregulated transcriptional programs that support malignant proliferation and survival. Casein kinase 1 alpha (CK1α) has been implicated in the regulation of p53 signaling and represents a potential therapeutic target. In this study, we aimed to investigate whether CK1α degradation induces broad transcriptomic changes in a p53-dependent manner. To address this, we performed RNA sequencing (RNA-seq) in two human AML cell lines with distinct TP53 status: MV4-11 (TP53 wild-type) and Kasumi-1 (TP53 mutant). Cells were treated with a CK1α degrader (PinA1) or vehicle control, followed by transcriptomic profiling. Comparative analysis was conducted to assess the extent and nature of gene expression changes induced by CK1α degradation. Notably, this study was designed to evaluate whether CK1α targeting leads to more pronounced transcriptional alterations in TP53 wild-type cells compared to TP53-mutant contexts. Our data provide insights into the p53-dependent transcriptional consequences of CK1α degradation and support its potential as a therapeutic strategy in AML.