作者: Chisato Tomida , Kana Aibara , Naoko Yamagishi , Chiaki Yano , Hikaru Nagano
DOI: 10.2152/JMI.62.195
关键词:
摘要: A number of anti-angiogenic drugs targeting vascular endothelial growth factor receptors (VEGF-R) have developed and enabled significant advances in cancer therapy including colorectal cancer. However, acquired resistance to the occurs, leading disease progression, such as invasion metastasis. How tumors become promote their malignancy remains fully uncertain. One possible mechanisms for progression may be direct effect VEGF-R inhibitors on tumor cells expressing VEGF-R. We investigated here a VEGF-R-targeting agent, regorafenib, which is first small molecule inhibitor VEGF-Rs treatment patients with cancer, phenotype changes colon HCT116 cells. Treatment regorafenib only 2 days activated cell migration invasion, while vehicle-treated control showed less activity. Intriguingly, chronic exposure 90 dramatically increased activities induced hypoxia-induced apoptosis. These results suggest that loss VEGF signaling induce VEGF/VEGF-R by gaining two major malignant phenotypes, apoptosis activation migration/invasion.