CCDC137 stabilizes S100A6 to activate the PI3K/AKT pathway and drive acute myeloid leukemia progression.

Coiled-coil domain-containing proteins (CCDCs) play pivotal roles in tumorigenesis by regulating gene transcription, apoptosis, and cell cycle progression. This study focuses on the function and mechanisms of CCDC137 in acute myeloid leukemia (AML). Our findings revealed that CCDC137 is significantly overexpressed in AML and is closely associated with poor patient prognosis. Functional experiments demonstrated that CCDC137 promotes cell proliferation and accelerates the cell cycle, thereby driving AML progression. Mechanistically, co-immunoprecipitation (Co-IP) experiments confirm the interaction between CCDC137 and S100A6, which significantly enhanced S100A6 protein stability. Stable S100A6 then activates the PI3K/AKT signaling pathway, thereby mediating the oncogenic effects of CCDC137. This study revealed the mechanism by which CCDC137 drives AML progression by stabilizing S100A6 and activating the PI3K/AKT pathway, thus providing a novel target for AML-specific therapy.