{"title":"Mesoporous Silica Nano-Modified Ginsenoside Rh2 Promote Tumor Immunosuppression and Inhibit Lung Cancer Development through the PD-1/PD-L1 Pathway.","authors":"Boxiong Cao, Qiang Wei, Hao Feng, Zemin He","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To explore the mechanism for mesoporous silica nano-modified ginsenoside Rh2 promoting tumor immunosuppression in lung cancer through PD-1/PD-L1 pathway.</p><p><strong>Methods: </strong>Firstly, G-Rh2-MSN were prepared and lung cancer A549 cells were cultured. The following groups were set up to analyze whether G-Rh2-MSN down-regulates PD-1/PD-L1 to promote tumor immunity, inhibit activities of lung cancer cells, and promote apoptosis: Model control group, G-Rh2 group, G-Rh2-MSN group, G-Rh2-MSN+PT001 group, G-Rh2-MSN+nivolumab group, G-Rh2-MSN+Durvalumab group, G-Rh2-MSN+atezolizumab group, and G-Rh2-MSN+nivolumab+Durvalumab group.</p><p><strong>Results: </strong>G-Rh2-MSN was successfully prepared and found to promote tumor immunity, inhibit the behaviors of lung cancer cells, and accelerate apoptosis. Down-regulation of PD-1/PD-L1 pathway by G-Rh2-MSN can accelerate development of tumor immunosuppressive lung cancer. G-Rh2-MSN promoted tumor immunity by downregulating PD-1/PD-L1, inhibiting activities of lung cancer cells, and promoting apoptosis.</p><p><strong>Conclusion: </strong>We clarified the mechanism for G-Rh2-MSN in lung cancer A549 cells, showing that it can significantly down-regulate PD-1/PD-L1 signaling, thereby promoting tumor immunity. G-Rh2-MSN modified material inhibits immune escape and reduces behaviors of lung cancer A549 cells by affecting PD-1 and PD-L1 expression, which has potential clinical application prospects.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"597-603"},"PeriodicalIF":1.1000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of clinical and laboratory science","FirstCategoryId":"3","ListUrlMain":"","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICAL LABORATORY TECHNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: To explore the mechanism for mesoporous silica nano-modified ginsenoside Rh2 promoting tumor immunosuppression in lung cancer through PD-1/PD-L1 pathway.
Methods: Firstly, G-Rh2-MSN were prepared and lung cancer A549 cells were cultured. The following groups were set up to analyze whether G-Rh2-MSN down-regulates PD-1/PD-L1 to promote tumor immunity, inhibit activities of lung cancer cells, and promote apoptosis: Model control group, G-Rh2 group, G-Rh2-MSN group, G-Rh2-MSN+PT001 group, G-Rh2-MSN+nivolumab group, G-Rh2-MSN+Durvalumab group, G-Rh2-MSN+atezolizumab group, and G-Rh2-MSN+nivolumab+Durvalumab group.
Results: G-Rh2-MSN was successfully prepared and found to promote tumor immunity, inhibit the behaviors of lung cancer cells, and accelerate apoptosis. Down-regulation of PD-1/PD-L1 pathway by G-Rh2-MSN can accelerate development of tumor immunosuppressive lung cancer. G-Rh2-MSN promoted tumor immunity by downregulating PD-1/PD-L1, inhibiting activities of lung cancer cells, and promoting apoptosis.
Conclusion: We clarified the mechanism for G-Rh2-MSN in lung cancer A549 cells, showing that it can significantly down-regulate PD-1/PD-L1 signaling, thereby promoting tumor immunity. G-Rh2-MSN modified material inhibits immune escape and reduces behaviors of lung cancer A549 cells by affecting PD-1 and PD-L1 expression, which has potential clinical application prospects.
期刊介绍:
The Annals of Clinical & Laboratory Science
welcomes manuscripts that report research in clinical
science, including pathology, clinical chemistry,
biotechnology, molecular biology, cytogenetics,
microbiology, immunology, hematology, transfusion
medicine, organ and tissue transplantation, therapeutics, toxicology, and clinical informatics.