RESUMO
To investigate the mechanism of 17β-estradiol (E2) induced tumor angiogenesis by VEGFα in the microenvironment of lung adenocarcinoma in A549 cells. Methods A549 cells were divided into three groups; PBS group, 10 nmol L"1 E2 group and 10 nmol L"1 E2 +5 (xmol L"1 estrogen receptor antagonist (ICI) group. Western blot was used to detect the expression of VEGFα in A549 cells, and ELISA was used to detect the expression of VEGFα in culture medium. The proliferation of human umbilical vein endothelial cells (HUVECs) was detected by MTT, the migration ability of HUVECs by scratch assay and the tubulogenesis in vitro by tube formation assay. Results Compared with control group, the expression of VEGFα in A549 cells in E2 group was higher, but the expression of VEGFα in A549 cells was significantly inhibited with the addition of ICI. Meanwhile, E2 induced the expression of VEGFα in A549 cells, promoting proliferation, migration and tubulogenesis of HUVEC, while ICI had the opposite effects. Conclusions E2 stimulates the expression of VEGFα by binding to estrogen receptor in A549 cells, promoting proliferation, migration and tube formation of HUVECs, contributing to lung adenocarcinoma angiogenesis.