Crenigacestat angiogenesis in SCLC is a key biological characteristic and an important mediator of tumor growth rate, invasiveness, and metastasis. Thus, the inhibition of angiogenesis is an effective method for the treatment of SCLC, and many targeted therapy drugs against angiogenesis, such as bevacizumab [36], cedirnnib

[37], and sorafenib [38], have widely been used in clinical practice. However, the therapeutic targets of these drugs are confined to VEGF-A and its receptor or signaling pathway. VEGF-A is a downstream target of HIF-1α, and it contains HREs with an HIF-1α binding site [39]. In our study, the expression of VEGF-A and the vascular reaction in the transplantation tumor was significantly inhibited after the expression of HIF-1α was downregulated by siHIF-1α. In addition to VEGF-A, there are many angiogenic factors that are directly or indirectly regulated see more by HIF-1α. Therefore, we propose that targeting HIF-1α may provide a broader inhibition

of tumor angiogenesis than targeting downstream angiogenesis factors of HIF-1α. In the future, we will conduct correlated research to confirm this proposal. Angiogenic factors regulated by HIF-1α in SCLC selleck chemicals cells transplantation tumor In pervious study although the multitude of insights were put into individual molecular effect on angiogenesis, such as increased migration and tube formation, which may be predicted to induce angiogenesis in vitro, these analyses in isolated systems clearly have their limitations, especially when a large scale of interconnections and complexity involved in the process of angiogenesis in vivo are considered. Allowing for this the in vivo expression of angiogenesis genes selected from the in vitro microarray analysis must be confirmed. Thus, it is important to successfully establish a simple and comprehensive model to test how HIF-1α regulates angiogenesis genes. Some scholars have suggested that xenograft models of tumor cells rely more on angiogenesis than naturally occurring

tumors and that the extent of angiogenesis is dependent on the site of implantation of the xenografts [40]. CAM is essentially a respiratory Tau-protein kinase membrane with a dense vascular net that maintains the blood-gas exchange. For abundant blood supply and a special anatomical position in the chick embryo, the CAM may provide more precise and convincing data for angiogenic factors than other in vivo experimental models [31]. Recent research and development for a targeted drug for SCLC has focused on inhibiting the expression of angiogenic factors, such as VEGF-A. However, the microenvironment of SCLC cell growth is largely hypoxic, and HIF-1α is the primary regulatory factor for angiogenesis. The factors that are mediated by HIF-1α and involved in angiogenesis of SCLC have not been previously reported. Therefore, in our study, we initially evaluated the effects of HIF-1α on the invasiveness of SCLC, which precedes angiogenesis.