Skip to main content
Fig. 1 | BMC Cancer

Fig. 1

From: Enhanced expression of Vastatin inhibits angiogenesis and prolongs survival in murine orthotopic glioblastoma model

Fig. 1

H1-Vastatin transfectd tumour cells specifically and suppressed MECs proliferation through paracrine inhibition. a H1 mediated gene transfections targeted only the tumour cells. Enhanced transcription level of Vastatin was only detected in the H1-Vastatin treated U87MG cells. b Proliferation curves of cells treated by H1-Vastatin or H1-EGFP. H1-Vastatin did not affected the proliferation of U87MG cells or MECs in separate culture condition. In the U87MG and MECs co-culure system, H1-Vastatin significantly suppressed the MECs growth on day 7 post treatment (P < 0.05). c Inhibition curves showing effects of different conditioned media (CM) on MECs proliferation. Conditioned medium from H1-Vastatin treated U87MG cells significantly decreased the cell viability of MECs in a dosage dependant way (* P < 0.05 against CM from H1-EGFP treated U87MG cells; # P < 0.05 against CM from H1-Vastatin treated MECs), suggesting Vastatin secreted by tumour cells inhibited neovascularization in paracrine manner

Back to article page