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人参基碳点通过增加铁死亡来抑制鳞状癌细胞的生长。

Ginseng-based carbon dots inhibit the growth of squamous cancer cells by increasing ferroptosis.

作者信息

Wang Zilin, Han Jing, Guo Zhiyong, Wu Hao, Liu Yige, Wang Wenying, Zhang Chenping, Liu Jiannan

机构信息

Department of Oral Maxillofacial - Head & Neck Oncology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai Research Institute of Stomatology, Shanghai, China.

College of Stomatology, Shanghai Jiao Tong University, Shanghai, China.

出版信息

Front Oncol. 2023 Mar 10;13:1097692. doi: 10.3389/fonc.2023.1097692. eCollection 2023.

DOI:10.3389/fonc.2023.1097692
PMID:36969027
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10036825/
Abstract

BACKGROUND

Recent studies indicated that Ginseng potentiate cancer treatments. Ginseng-based carbon dots (GCDs) might possess properties to kill cancer cells and inhibit malignant tumor development and invasion. This study aimed to prepare GCDs, examine their effects on cancer cell growth and invasion, and explore the mechanisms involved.

METHODS

GCDs were synthesized, purified, and characterized. Cells were cultured with GCDs and were tested for growth, invasiveness, and wound healing. RNA was extracted for transcriptomics analysis. Protein expression was evaluated using western blot and immunohistochemistry. Mice were injected with cancer cells and treated with PBS or GCDs. Tumor volume was evaluated.

RESULTS

GCDs were successfully synthesized and purified. The solution was yellow under sunlight and fluorescent blue under ultraviolet light. Electron microscopy showed GCDs with a uniform shape without apparent aggregation and an average diameter of about 4 nm. GCDs inhibited Cal-27, SCC-25, and SCC-7 cancer cell growth at concentrations of >250-300 μg/mL, while GCDs inhibited the non-cancerous HaCaT cells at concentrations >400 μg/mL. Immunofluorescence showed that GCDs could enter the cells. Transcriptomics revealed 552 downregulated mRNAs and 338 upregulated ones, including mRNAs involved in the oxidative phosphorylation and ferroptosis pathways. GCDs induced the ferroptosis of cancer cells, as shown by decreased GPX-4 and increased COX-2. GCDs decreased cell invasion and migration. , GCDs decreased tumor growth without apparent organ toxicity and promoted CD4 T cell infiltration in the tumor.

CONCLUSION

GCDs appear to possess anticancer properties by increasing ferroptosis, resulting in cancer cell growth inhibition and .

摘要

背景

最近的研究表明,人参可增强癌症治疗效果。基于人参的碳点(GCDs)可能具有杀死癌细胞、抑制恶性肿瘤发展和侵袭的特性。本研究旨在制备GCDs,研究其对癌细胞生长和侵袭的影响,并探索其相关机制。

方法

合成、纯化并表征GCDs。将细胞与GCDs一起培养,并检测其生长、侵袭和伤口愈合情况。提取RNA进行转录组学分析。使用蛋白质印迹法和免疫组织化学法评估蛋白质表达。给小鼠注射癌细胞,并用磷酸盐缓冲液(PBS)或GCDs进行治疗。评估肿瘤体积。

结果

成功合成并纯化了GCDs。该溶液在阳光下呈黄色,在紫外线下呈荧光蓝色。电子显微镜显示GCDs形状均匀,无明显聚集,平均直径约为4nm。当浓度>250-300μg/mL时,GCDs抑制Cal-27、SCC-25和SCC-7癌细胞的生长,而当浓度>400μg/mL时,GCDs抑制非癌细胞HaCaT细胞的生长。免疫荧光显示GCDs可进入细胞。转录组学分析显示有552个mRNA下调,338个mRNA上调,包括参与氧化磷酸化和铁死亡途径的mRNA。GCDs诱导癌细胞发生铁死亡,表现为谷胱甘肽过氧化物酶4(GPX-4)减少和环氧合酶-2(COX-2)增加。GCDs减少细胞侵袭和迁移。此外,GCDs可减少肿瘤生长,且无明显器官毒性,并促进肿瘤中CD4 T细胞浸润。

结论

GCDs似乎通过增加铁死亡而具有抗癌特性,从而抑制癌细胞生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/43620b015b4e/fonc-13-1097692-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/7bdda5f04b54/fonc-13-1097692-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/80349fd41f98/fonc-13-1097692-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/25162ab6a590/fonc-13-1097692-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/38dc47c79596/fonc-13-1097692-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/c6f743f70e6b/fonc-13-1097692-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/43620b015b4e/fonc-13-1097692-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/7bdda5f04b54/fonc-13-1097692-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/80349fd41f98/fonc-13-1097692-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/25162ab6a590/fonc-13-1097692-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/38dc47c79596/fonc-13-1097692-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/c6f743f70e6b/fonc-13-1097692-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b286/10036825/43620b015b4e/fonc-13-1097692-g006.jpg

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