Fig. 7From: Underlying mechanisms and drug intervention strategies for the tumour microenvironmentIntervention of combined drugs on the TME. Rapamycin (RapA) is a mTOR inhibitor that inhibits tumour proliferation through anti-angiogenesis and can be enhanced in combination with cisplatin. Cisplatin combined with paclitaxel inhibits tumour invasion. The combination of everolimus and sunitinib can affect stromal cells and cancer cells in the TME. Antiangiogenic drugs (AADs) combined with carnitine palmitoyltransferase 1A (CPT1) inhibitors significantly inhibited fatty acid oxidation (FAO) -induced cell proliferation and angiogenesis. Ginsenoside Rg3 combined with cisplatin can inhibit epithelial-mesenchymal transition (EMT) of tumour cells. Hedgehog (HH) signalling pathway inhibitors combined with bufalin can inhibit tumour proliferation. Tranilast can dow-regulate CAF activity, promote vascular normalization, and help docetaxel micelles (DTX-ms) reach tumour tissue through veins and kill tumour cells. Sorafenib combined with bufalin affects the tumour vascular microenvironment through targeting the mTOR/VEGF signalling pathwayBack to article page