Project description:Triple negative breast cancer (TNBC) poorly responds to immune checkpoint blockade (ICB) therapy. Dormant tumor cells are recognized as immunotherapy-resistant reservoirs, potential leading to tumor relapse, highlighting the importance to elucidate the mechanisms underlying immunotherapy resistance. Herein, we demonstrated that dormant tumor cells were resistant to ICB therapy and occupied an immunosuppressive niche with enhanced tumor-associated macrophages (TAMs) and decreased CD8+T cells infiltration in mouse TNBC allografts via a label-retention system. CEBPB was highly expressed in dormant tumor cells and maintained tumor dormancy by transcriptionally activating cell cycle negative regulators like CCNG2 and p27.
Project description:Triple negative breast cancer (TNBC) poorly responds to immune checkpoint blockade (ICB) therapy. Dormant tumor cells are recognized as immunotherapy-resistant reservoirs, potential leading to tumor relapse, highlighting the importance to elucidate the mechanisms underlying immunotherapy resistance. Herein, we demonstrated that dormant tumor cells were resistant to ICB therapy and occupied an immunosuppressive niche with enhanced tumor-associated macrophages (TAMs) and decreased CD8+T cells infiltration in mouse TNBC allografts via a label-retention system. CEBPB was highly expressed in dormant tumor cells and maintained tumor dormancy by transcriptionally activating cell cycle negative regulators like CCNG2 and p27.
Project description:CEBPB contributes to the migration of breast cancer cells. We used microarrays to detail the mechanism of CEBPB with downstream targets that drive breast cancer cell migration. CEBPB were overexpressed in MDA-MB231 cell for RNA extraction and hybridization on Agilent microarrays. We sought to obtain the mechanisms of CEBPB with downstream proteins that drive breast cancer cell migration.
Project description:CEBPB contributes to the migration of breast cancer cells. We used microarrays to detail the mechanism of CEBPB with downstream targets that drive breast cancer cell migration.