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黄芪多糖通过降低肝癌细胞中的 O-GlcNAc 糖化促进阿霉素诱导的细胞凋亡。

Astragalus Polysaccharide Promotes Doxorubicin-Induced Apoptosis by Reducing O-GlcNAcylation in Hepatocellular Carcinoma.

机构信息

School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.

Department of Pharmacology, School of Medicine, Sun Yat-sen University, Shenzhen 518107, China.

出版信息

Cells. 2023 Mar 10;12(6):866. doi: 10.3390/cells12060866.

DOI:10.3390/cells12060866
PMID:36980207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10047337/
Abstract

The toxicity and side effects of chemotherapeutic drugs remain a crucial obstacle to the clinical treatment of hepatocellular carcinoma (HCC). Identifying combination therapy from Chinese herbs to enhance the sensitivity of tumors to chemotherapeutic drugs is of particular interest. Astragalus polysaccharide (APS), one of the natural active components in Astragalus membranaceus, has been reported to exhibit anti-tumor properties in diverse cancer cell lines. The aim of this study was to determine the effect of APS on Doxorubicin (Dox)-induced apoptosis in HCC and the underlying mechanism. The results showed that APS dose-dependently promoted Dox-induced apoptosis and enhanced endoplasmic reticulum (ER) stress. Additionally, APS decreased the mRNA level and protein stability of O-GlcNAc transferase (OGT), and increased the O-GlcNAcase (OGA) expression. Furthermore, OGT lentiviral transfection or PugNAc (OGA inhibitor) treatment reversed the ER stress and apoptosis induced by the combination of Dox and APS. A xenograft tumor mouse model confirmed that the combination of APS and Dox showed an advantage in inhibiting tumor growth in vivo. These findings suggested that APS promoted Dox-induced apoptosis in HCC cells through reducing the O-GlcNAcylation, which led to the exacerbation of ER stress and activation of apoptotic pathways.

摘要

化疗药物的毒性和副作用仍然是肝细胞癌（HCC）临床治疗的一个关键障碍。从中药中寻找联合治疗方法来提高肿瘤对化疗药物的敏感性特别受到关注。黄芪多糖（APS）是黄芪中的一种天然活性成分，已被报道在多种癌细胞系中具有抗肿瘤特性。本研究旨在确定 APS 对阿霉素（Dox）诱导的 HCC 细胞凋亡的影响及其潜在机制。结果表明，APS 呈剂量依赖性地促进 Dox 诱导的细胞凋亡，并增强内质网（ER）应激。此外，APS 降低了 O-连接的 N-乙酰葡萄糖胺转移酶（OGT）的 mRNA 水平和蛋白稳定性，并增加了 O-糖苷酶（OGA）的表达。此外，OGT 慢病毒转染或 PugNAc（OGA 抑制剂）处理逆转了 Dox 和 APS 联合诱导的 ER 应激和细胞凋亡。在异种移植肿瘤小鼠模型中证实，APS 和 Dox 的联合应用在体内抑制肿瘤生长方面具有优势。这些发现表明，APS 通过减少 O-糖基化来促进 HCC 细胞中 Dox 诱导的细胞凋亡，导致 ER 应激加剧和凋亡途径激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/af21a198d342/cells-12-00866-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/af1e159c4b4a/cells-12-00866-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/39dc69293bd3/cells-12-00866-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/a1b13c064203/cells-12-00866-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/408aa3ea4d5c/cells-12-00866-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/57b24afc871e/cells-12-00866-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/af21a198d342/cells-12-00866-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/af1e159c4b4a/cells-12-00866-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/39dc69293bd3/cells-12-00866-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/a1b13c064203/cells-12-00866-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/408aa3ea4d5c/cells-12-00866-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/57b24afc871e/cells-12-00866-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37ab/10047337/af21a198d342/cells-12-00866-g006.jpg

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