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低糖通过抑制肝癌细胞自噬促进 CD133mAb 诱导的细胞死亡。

Low glucose promotes CD133mAb-elicited cell death via inhibition of autophagy in hepatocarcinoma cells.

机构信息

International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, The Second Military Medical University, 225 Changhai Road, Shanghai 200438, China.

出版信息

Cancer Lett. 2013 Aug 9;336(1):204-12. doi: 10.1016/j.canlet.2013.04.031. Epub 2013 May 4.

DOI:10.1016/j.canlet.2013.04.031
PMID:23652197
Abstract

CD133 on cancer stem cells is a potential therapeutic target. In this study, CD133 antibody (CD133mAb) treatment resulted in cell death in hepatoma LM3, HepG2, Hep3B and Huh-7 cells, especially under low glucose condition. The treatment also inhibited formation of spheroids, colonies, and xenograft tumors. Ectopic CD133 enabled hepatocyte L02 to be suppressed by CD133mAb and increased spheroid formation. CD133mAb caused cell death in primary HCC cells and sensitized them to Doxorubicin and Cisplatin. The antibody effect was attributed to suppressing autophagy and promoting necrotic cell death. Therefore, targeting CD133 under low glucose condition is a potential therapeutic approach for hepatocarcinomas.

摘要

CD133 蛋白在肿瘤干细胞上的表达是一个潜在的治疗靶点。本研究中,CD133 抗体(CD133mAb)治疗导致肝癌 LM3、HepG2、Hep3B 和 Huh-7 细胞死亡,尤其在低糖条件下。该治疗还抑制了球体、集落和异种移植瘤的形成。外源性 CD133 使肝细胞 L02 能够被 CD133mAb 抑制,并增加球体形成。CD133mAb 导致原代 HCC 细胞死亡,并增加其对阿霉素和顺铂的敏感性。抗体的作用归因于抑制自噬和促进坏死性细胞死亡。因此,在低糖条件下靶向 CD133 是一种潜在的肝癌治疗方法。

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