Endocytosis of ATB0,+(SLC6A14)-targeted liposomes for drug delivery and its therapeutic application for pancreatic cancer

内吞作用 内化 脂质体 胰腺癌 药物输送 细胞毒性 吉西他滨 内体 靶向给药 毒品携带者 癌细胞 药理学 化学 药品 癌症研究 生物化学 赖氨酸 癌症 体外 氨基酸 医学 细胞 内科学 有机化学
作者
Longfa Kou,Huirong Huang,Xinlu Lin,Xinyu Jiang,Yi Wang,Qiuhua Luo,Jin Sun,Qing Yao,Vadivel Ganapathy,Ruijie Chen
出处
期刊:Expert Opinion on Drug Delivery [Informa]
卷期号:17 (3): 395-405 被引量:28
标识
DOI:10.1080/17425247.2020.1723544
摘要

Background SLC6A14 (ATB0,+), a Na+/Cl–coupled transporter for neutral/cationic amino acids, is overexpressed in many cancers; It has been investigated as a target for improved liposomal drug delivery to treat liver cancer.Research design and methods Here we explored the mechanism of ATB0,+-mediated entry of such liposomes. As ATB0,+ is highly expressed in pancreatic cancer, we also examined the therapeutic utility of ATB0,+-targeted liposomal drug delivery to treat this cancer.Results The uptake of lysine-conjugated liposomes (LYS-LPs) was greater in ATB0,+-positive MCF7 cells. The uptake process consisted of two steps: binding and internalization. The binding of LYS-LPs to MCF7 cells was higher than that of bare liposomes, and the process was dependent on Na+ and Cl−, and inhibitable by ATB0,+ substrates or blocker. In contrast, the internalization step was independent of lysine. The cellular entry of LYS-LPs facilitated by ATB0,+ occurred via endocytosis with transient endosomal degradation of ATB0,+ protein with subsequent recovery. Moreover, LYS-LPs also enhanced the uptake and cytotoxicity of gemcitabine in these cells in an ATB0,+-dependent manner.Conclusions We conclude that ATB0,+ could be exploited for targeted drug delivery in the form of lysine-conjugated liposomes and that the approach represents a novel strategy for enhanced pancreatic cancer therapy.
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