GSE201381
Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca
How to identify subgroups of PCa patients for immune checkpoint therapy (ICT) remains not fully understood. Basic helix-loop-helix family member e22 (Bhlhe22) is upregulated in bone metastatic PCa and drives an immunosuppressive bone TME. Tumoral Bhlhe22 mediates the high expression of colony stimulating factor 2 (CSF2), which results in the infiltration of myeloid-derived suppressor cells (MDSCs) and prolonged immunocompromised T cell status. Here, we reveal the immunosuppressive mechanism of tumoral Bhlhe22 and provide a prospective ICT combination therapeutic for Bhlhe22+ PCa patients. Overall design: Differential gene expression profile between control (RM-1-Vector) cells and Bhlhe22 overexpression (RM-1-Bhlhe22) cells.