Fig. 3
From: Underlying mechanisms and drug intervention strategies for the tumour microenvironment
Intervention of targeted therapy on the TME. Regorafenib inhibits the interaction between mesenchymal stem cells (MSCs) and cancer cells. Rapamycin-mediated autophagy can reduce the expression of Bcl-2 and survivin and increase the expression of Smac in TAMS. Apatinib can reduce cancer angiogenesis and inhibit the expression of PD-L1 through targeted STAT3 inhibition of the EMT and blockade of the PI3K/AKT and VEGFR2/RAF/MEK/ERK signalling pathways, thus affecting VEGF-mediated cell proliferation and invasion. WRG-28 inhibits cancer invasion and migration by targeting DDR2. Dasatinib reduced the M2 polarization of TAMS. Bortezomib (BTZ) and phenobarbital (PST) can reduce the survival rate of CAFs and inhibit the proliferation of cancer cells by inducing caspase-3-mediated apoptosis. The inhibition of apelin can inhibit angiogenesis and growth, and reduce the infiltration of suppressor cells derived from the polymorphonuclear myeloid system