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负载提取物的间充质干细胞条件培养基衍生外泌体通过调节NF-κB和MAPK通路抑制肺癌

Mesenchymal Stem Cell-Conditioned Media-Derived Exosomes Loaded With Extract Inhibit Lung Cancer via NF-κB and MAPK Pathway Modulation.

作者信息

Zhu Cailin, Shang Dong

机构信息

Department of Thoracic Surgery The First Affiliated Hospital of Xi'an Jiaotong University Xi'an China.

Department of Respiratory and Critical Care Medicine The First Affiliated Hospital of Xi'an Jiaotong University Xi'an China.

出版信息

Food Sci Nutr. 2025 Aug 20;13(8):e70802. doi: 10.1002/fsn3.70802. eCollection 2025 Aug.

DOI:10.1002/fsn3.70802
PMID:40852159
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12368280/
Abstract

The increasing prevalence of drug resistance diminishes the efficacy of chemotherapy and other therapeutic modalities for individuals diagnosed with lung cancer. Therefore, it is imperative to develop novel treatment approaches. This study examined how mesenchymal stem cell-derived exosomes containing extraction of () affected lung cancer cells. Exosomes were obtained from mesenchymal stem cells and loaded with extract (extract-exosomes) by sonication. The effects of extract-exosomes on A549 lung cancer cells were assessed in vitro on cell viability, colony formation, mitochondrial membrane disruption, migration, apoptosis, autophagy, and cell cycle. Moreover, we examined apoptosis-related genes mRNA expression by real-time PCR. Finally, both NF-κB and MAPK signaling pathways were evaluated by western blotting method. Our results indicated that exposure to extract-exosomes significantly inhibits lung cancer cells proliferation, colony formation, and migration. Furthermore, this treatment increased mitochondrial membrane disruption, apoptosis, and autophagy in the cancer cells. Additionally, there was a notable increase in the number of the treated cancer cells at G1 and sub-G1 phases of the cell cycle. The research findings indicate that extract-exosomes can inhibit lung cancer cells proliferation through the induction of apoptosis and autophagy, cell cycle arrest, as well as modification of NF-κB and MAPK pathways.

摘要

耐药性的日益普遍降低了化疗和其他治疗方式对肺癌患者的疗效。因此,开发新的治疗方法势在必行。本研究探讨了含有()提取物的间充质干细胞衍生外泌体如何影响肺癌细胞。外泌体从间充质干细胞中获得,并通过超声处理加载提取物(提取物 - 外泌体)。在体外评估提取物 - 外泌体对A549肺癌细胞的细胞活力、集落形成、线粒体膜破坏、迁移、凋亡、自噬和细胞周期的影响。此外,我们通过实时PCR检测凋亡相关基因的mRNA表达。最后,通过蛋白质印迹法评估NF-κB和MAPK信号通路。我们的结果表明,暴露于提取物 - 外泌体可显著抑制肺癌细胞的增殖、集落形成和迁移。此外,这种处理增加了癌细胞中线粒体膜破坏、凋亡和自噬。此外,在细胞周期的G1期和亚G1期,处理后的癌细胞数量显著增加。研究结果表明,提取物 - 外泌体可通过诱导凋亡和自噬、细胞周期阻滞以及改变NF-κB和MAPK途径来抑制肺癌细胞的增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/36114fcb0300/FSN3-13-e70802-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/8b2a6313a951/FSN3-13-e70802-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/9680255f62a0/FSN3-13-e70802-g009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/36114fcb0300/FSN3-13-e70802-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/99e3d08717b1/FSN3-13-e70802-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/00fa627248ed/FSN3-13-e70802-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/af1d178064a1/FSN3-13-e70802-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/9ee9a49cbe82/FSN3-13-e70802-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/95fc77f1db82/FSN3-13-e70802-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/01994c9090f4/FSN3-13-e70802-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/4ade49510bd1/FSN3-13-e70802-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/8b2a6313a951/FSN3-13-e70802-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/9680255f62a0/FSN3-13-e70802-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/cb99d7a46238/FSN3-13-e70802-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/8f07e9e845df/FSN3-13-e70802-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f826/12368280/36114fcb0300/FSN3-13-e70802-g006.jpg

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