Fig. 1
From: Advances in immunotherapy for triple-negative breast cancer
Interactions between components of TME induce therapeutic resistance in TNBC. The hypoxia of TME induces the activation of LOX and reshapes the ECM, leading to the formation of chemotherapy resistance. The activation of the P4H-α1/HIF-1 axis has been found to enhance the stemness of TNBC cells, resulting in a reduction in OXPHOS and ROS. CAF-induced lipid-associated macrophages induce immunosuppression of TNBC. The adipocytes induce the production of oleic acid to result in the protection of TNBC cells from ferroptosis by ACSL3. The M2 macrophages secrete VEGF and activate PCAT6 to promote the proliferation and metastasis of tumor cells through the modulation of VEFGR2