Tumor growth and metastasis are closely related to tumor angiogenesis, and the combination of angiogenesis inhibitor and interventional therapy opens up a new way for the treatment of vascular-rich tumors. A large number of studies have shown that tumor growth needs blood vessels to provide nutrition, without blood vessels to supply blood the tumor will not grow, and the maximum volume of its growth can only be 2mm³~3mm³; the large number of blood vessels in the tumor creates favorable conditions for tumor growth and metastasis, and is also one of the main reasons for the failure of clinical treatment of tumors [1]. Therefore, anti-tumor angiogenesis has an extremely important value in tumor treatment. This paper briefly reviews the issue of angiogenesis inhibitors and tumor intervention as follows. 1. Tumor angiogenesis 1. 1 Mechanism In 1971, Folkman [2] discovered that tumor growth was vascular-dependent and proposed the hypothesis that anti-tumor angiogenesis could treat tumors. Many studies have shown that tumor angiogenesis is a complex process involving multiple factors and the basic steps [3]: (i) release of angiogenesis-stimulating factors from tumor tissue; (ii) perivascular extracellular matrix remodeling and basement membrane degradation; (iii) endothelial cell proliferation and migration; and (iv) neovascularization, etc. Tumor angiogenesis is controlled by positive and negative regulators [4]: when positive regulators, such as fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF), are upregulated to initiate the angiogenic mechanism; negative regulators, such as angiostation, endiostation, platelet factor-4 (PF-4 ), etc., play an inhibitory role in angiogenesis. The concept of “angiogenic switch” was introduced when studying these regulatory factors that regulate tumor angiogenesis [5]. It is turned on during tumorigenesis, and during the latent phase of tumor, the positive and negative factors remain in dynamic balance, i.e., in a dormant state. 1.2 Effects of angiogenesis on tumor growth, metastasis and prognosis Tumor growth requires blood supply to obtain nutrients and oxygen. In the pre-angiogenic stage of tumor growth, there is no new angiogenesis and the tumor mainly relies on cellular diffusion to obtain oxygen and nutrients; in the angiogenic stage, the tumor can grow exponentially due to angiogenesis in the tumor and make distant metastasis possible [3]. Tumor metastasis is a complex multi-step process that can be divided into [6]: ① tumor cells detach from the primary focus; ② degrade the basement membrane to infiltrate outward, migrate and adhere to vascular endothelial cells; ③ enter the circulatory system to reach and stay in the distant vessel wall with blood flow; ④ cross the vessel wall and enter the extracellular matrix, and finally form metastatic foci in specific tissues or organs. In addition, dysregulation of various molecular mechanisms (e.g., growth factors, cytokines, protein hydrolysis systems) in the microenvironment surrounding the primary tumor is intrinsic to tumor microangiogenesis and the development of metastases [7]. The structural lack of smooth muscle cells and nerve endings in the neointimal tissue and the incomplete endothelial basement membrane make it easy for tumor cells to penetrate. The more the number of microvessels, the more chances for tumor cells to enter the blood circulation, and the number of tumor vascular endothelial cells dividing is 50 times more than normal endothelial cells, making tumor tissues extremely easy to form new vascular networks, while the neovascular network provides channels for tumor metastasis and more nutrients for tumor growth, thus forming a vicious circle of alternating cause and effect. Furthermore, angiogenesis itself has certain tissue infiltration, and tumor cells can invade along the collagen fissures opened by neovascularization. The metastases formed by invasion are positively correlated with the total number of tumor cells entering the vasculature [8]. In measuring the extent of tumor angiogenesis, microvessel density count is a representative quantitative index [9]. An increase in tumor microvessel density (MVD) is also associated with a significant increase in malignant potential such as tumor invasion and metastasis. The administration of hematopoietic inhibitors can significantly inhibit tumor growth and metastasis, reduce microvessel density, and improve the prognosis of tumor-bearing animals and patients.Grew et al [10] suggested that the quantitative detection of VEGF in urine can be used as a differential diagnosis of bladder tumors and an indicator for early diagnosis of postoperative recurrence.Both VEGF and MVD are effective indicators for determining the prognosis of breast cancer, and among them, MVD may be an independent factor for determining the prediction of breast cancer [11]. VEGF and MVD are both effective prognostic indicators for breast cancer, and MVD may be an independent factor in predicting breast cancer [11]. The development of angiogenesis inhibitors to control tumor growth and metastasis has become a new initiative in tumor prevention and treatment [2]: (i) blocking the ability of endothelial cells to degrade the surrounding stroma; (ii) directly inhibiting the function of endothelial cells; (iii) blocking the synthesis and release of angiogenic factors and antagonizing their effects; (iv) blocking the behavior of integrins on the surface of endothelial cells. behavior of endothelial cells. Several agents with anti-angiogenic properties have been developed, mainly in two main categories [12]: the first category is specific agents, i.e., they can specifically inhibit tumor vascular endothelial cells, but have no effect on non-endothelial cells, such as TNP-470, Angiostation, PF-4, Endiostation, etc. The second category is non-specific inhibitors, i.e. angiogenesis inhibitors that inhibit both endothelial cells and tumor cells, such as IL-12, IFN, etc. IL-12 activates T cells and NK cells to secrete IFN-α, which improves phagocytic killing capacity and is less toxic, and has anti-tumor angiogenic effects [13]. From the perspective of anti-cancer, the second class of drugs is more superior, which can control the blood supply of tumors and have toxic effects on tumor cells, but also produce many side effects on non-tumor cells [5], thus limiting the long-term application in clinical practice. Interventional radiology (IVR) is the third major clinical treatment technology that is developing rapidly after internal medicine and surgery [14]. Interventional radiology plays a very important role in the treatment of tumor. In China, some interventional techniques for tumors have been carried out one after another; Chen Xinrong, Liu Zijiang and Lin Gui first introduced bronchial artery perfusion for lung cancer in the early 80s, and then other interventional tumors were also flourished, and the most successful one is hepatic artery embolization/chemotherapy for hepatocellular carcinoma, which has become the first choice for middle and late stage hepatocellular carcinoma. Interventional therapy is an indispensable and important tool in the comprehensive treatment of tumors [15]. Nevertheless, at present, the efficacy of various methods used to treat tumors alone is not satisfactory, and the same applies to tumor interventional therapy, and there are still problems such as microcatheter materials, operation techniques, perfusion drugs, embolic substances, etc. that need further improvement. 3.2 Comprehensive application of angiogenesis inhibitors in tumor interventional therapy As the research on tumor angiogenesis inhibitors continues to deepen and the scope of clinical trials gradually widens, angiogenesis inhibitors have the following advantages compared with conventional chemotherapeutic drugs that directly kill tumor cells [16]: ① Angiogenesis inhibitors act directly on vascular endothelial cells, while conventional anticancer drugs are affected by tissue necrosis, fibrosis and intra-tissue hypertension when they spread through tissues. (2) Vascular endothelial cells are normal cells with stable genotypes, which are less prone to drug resistance, while tumor genotypes are unstable and prone to drug resistance; (3) Vascular endothelial cells in primary and secondary tumors are the same, but the biological behaviors of tumor cells in primary and secondary foci are different, and the response to chemotherapy is different; (4) Tumor vascular endothelial cells proliferate many times faster than normal tissues. The effect of angiogenesis inhibitors on normal tissues is mild. If combined with surgery, radiotherapy, conventional chemotherapy and intervention, they have stronger anti-tumor effects than single means. In particular, interventional radiology uses catheter technology to selectively or super-selectively insert direct blood supply vessels to the tumor, perfusion or perfusion plus embolization and installation of chemotherapy pumps, which can increase local drug concentrations in the tumor while systemic drug concentrations are low, with fewer side effects. significantly better than HAL or TNP-470 treatment alone, with reduced tumor vascular density and greatly reduced peritumor collateral vessels. Angiostation and Endostation are two of the most potent inhibitors of angiogenesis [9]. 1997 O’Reilly [18] demonstrated that Endostation inhibits metastasis and primary implantation of tumors.Endostation is an endogenous inhibitor of angiogenesis, and protein hydrolase Endostation is produced after hydrolysis of collagen X VIII. Collagen X VIII was detected in 57 liver cancer tissues, and it was found that cases with high levels had smaller tumors and low MVD and a low recurrence rate within 2 years after surgery [19]. If the combined intervention of Angiostation and Endostation factor could be a boon for tumor patients. Marimastat (BB-2516), which has been used in phase III clinical studies for the treatment of pancreatic cancer, non-small cell lung cancer and breast cancer [2], will have better results when combined with interventional means. α-Interferon (IFN-α) is newly used as an angiogenesis inhibitor that blocks angiogenic factors and is in phase II and III clinical studies by inhibiting FGF into VEGF production. TNP-470 can TNP-470 strongly inhibits vascular endothelial cell proliferation and has been used clinically [20]. IL-12 enhances p10 production induced by pro-angiogenic inhibitors and has anti-tumor angiogenic function. Application of a recombinant adenovirus encoding the murine IL-12 gene in an encoded murine model revealed that IL-12 significantly inhibited tumor growth, an effect independent of immune attack [21]. In combination with interventional therapies, more satisfactory results can be achieved.VEGF is more significantly elevated around necrotic and hypoxic areas within the tumor, and elevated VEGF levels were observed after TACE [22]. Inhibition of hepatocellular carcinoma growth was observed by blocking its pro-angiogenic effect using VEGF antisense cDNA [23]. Making full use of the respective advantages of tumor angiogenesis inhibitors directly and efficiently inhibiting tumor blood vessel formation and conventional chemotherapeutic agents directly killing tumor cells, combined with the advantages of interventional minimally invasive, rapid and efficient treatment of tumors is undoubtedly a new breakthrough in tumor interventional therapy. It makes tumor shrinkage and then surgical resection possible, while reducing anemia symptoms and surgical blood loss. 4. Problems and outlook Inhibition of tumor angiogenesis is an important anti-tumor strategy [24], but it is still in the early stage of trial, and it is difficult to evaluate its clinical value comprehensively [25], and further research and exploration of basic theory and clinical application are needed, some mechanisms have not been clearly elucidated, and the assessment of clinical research and value still lacks a large number of case reports. It is envisioned that combining angiogenesis inhibitors with microencapsulation and/or radionuclide labeling techniques may be expected to be a better integrated oncologic interventional therapy. With the success of human genetic mapping, the continuous progress of human genome project and the continuous improvement of molecular biology technology, we believe that there will be revolutionary breakthroughs in interventional tumor treatment and the process of human tumor conquest will be greatly shortened.