Angiotensin 1-7 Overexpression Mediated by a Capsid-optimized AAV8 Vector Leads to Significant Growth Inhibition of Hepatocellular Carcinoma In vivo.
作者： Yingying Mao , Nana Pei , Xinglu Chen , Huiying Chen , Renhe Yan
DOI: 10.7150/IJBS.22235
关键词: Chemistry 、 Angiogenesis 、 In vivo 、 Growth inhibition 、 Cancer research 、 Adeno-associated virus 、 Hepatocellular carcinoma 、 PIGF 、 Gene delivery 、 Vascular endothelial growth factor A
摘要: Background: Angiotensin-(1-7) [Ang-(1-7)] has been identified to inhibit the growth of many types tumor cells both in vitro and vivo. However, rapid degradation Ang-(1-7) vivo limits its clinical application. Adeno-associated virus (AAV) serotype-8 is a remarkable vector for long-term gene delivery. Method: This study was designed investigate effects AAV-mediated overexpression on hepatocellular carcinoma. We first generated three different tyrosine (Y) phenylalanine (F) mutants AAV8 (Y447F, Y703F, Y708F) evaluated their transduction efficiencies. Results: The data indicated that Y703F mutant elicited significant enhancement liver delivery when compared with wild-type (wtAAV8). anti-tumor effect mediated by this optimized H22 hepatoma-bearing mice. Our results demonstrated AAV-Ang-(1-7) persistently inhibited carcinoma significantly downregulating angiogenesis. confirmed observed decreases levels proangiogenic factors VEGF PIGF. Conclusion: Collectively, these suggest may be an effective alternative therapy due activity.
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