作者: Wonyoung Kang , Sung Heon Kim , Hee Jin Cho , Juyoun Jin , Jeongwu Lee
关键词: Pathology 、 Cancer research 、 Phenotype 、 Stem cell 、 Bevacizumab 、 Angiogenesis 、 Gene expression profiling 、 In vivo 、 Transcriptome 、 Medicine 、 Epithelial–mesenchymal transition
摘要: Glioblastoma multiforme (GBM) possesses florid angiogenesis. However, the anti-angiogenic agent, Bevacizumab, did not improve overall survival of GBM patients. For more durable treatment, we interrogated resistant mechanisms against Bevacizumab. Serial orthotopic transplantation in vivo Bevacizumab-treated cells provoked complete refractoriness to treatment. These tumors were also highly enriched with malignant phenotypes such as invasiveness, epithelial mesenchymal transition, and stem-like features. Through transcriptome analysis, identified that Talin1 (TLN1) significantly increased refractory GBMs. Inhibition TLN1 only attenuated characteristics but reversed resistance Bevacizumab data implicate a novel therapeutic target for overcome therapies.