Activation of KIT Signaling Promotes Early Tumorigenesis through AP-1 pathway in APC/TP53 Double-Knockout Human Colon Organoids
This study investigates the role of KIT signaling in the early stages of colorectal cancer (CRC) using a CRISPR-Cas9-engineered human colon organoid model with simultaneous APC and TP53 knockouts. By integrating multi-omics data, the research identifies a novel AP-1/KIT signaling axis driving early tumorigenic processes. The findings highlight KIT as a key oncogenic driver, activated by AP-1 transcription factors, enhancing MAPK and Wnt pathways to sustain tumor cell proliferation. Pharmacological inhibition of AP-1 suppresses tumorigenic features, offering potential therapeutic implications for CRC treatment.
This study investigates the role of KIT signaling in the early stages of colorectal cancer (CRC) using a CRISPR-Cas9-engineered human colon organoid model with simultaneous APC and TP53 knockouts. By integrating multi-omics data, the research identifies a novel AP-1/KIT signaling axis driving early tumorigenic processes. The findings highlight KIT as a key oncogenic driver, activated by AP-1 transcription factors, enhancing MAPK and Wnt pathways to sustain tumor cell proliferation. Pharmacological inhibition of AP-1 suppresses tumorigenic features, offering potential therapeutic implications for CRC treatment.
Cancer Genomics Research Laboratory