Streptococcus pneumoniae promotes lung cancer development and progression
Summary: Streptococcus pneumoniae (SP) is associated with lung cancer, yet its role in the tumorigenesis remains uncertain. Herein we find that SP attaches to lung cancer cells via binding pneumococcal surface protein C (PspC) to platelet-activating factor receptor (PAFR). Interaction between PspC a...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2023-02-01
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| Series: | iScience |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2589004222021964 |
| _version_ | 1828012388610211840 |
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| author | Ning Li Huifen Zhou Van K. Holden Janaki Deepak Pushpa Dhilipkannah Nevins W. Todd Sanford A. Stass Feng Jiang |
| author_facet | Ning Li Huifen Zhou Van K. Holden Janaki Deepak Pushpa Dhilipkannah Nevins W. Todd Sanford A. Stass Feng Jiang |
| author_sort | Ning Li |
| collection | DOAJ |
| description | Summary: Streptococcus pneumoniae (SP) is associated with lung cancer, yet its role in the tumorigenesis remains uncertain. Herein we find that SP attaches to lung cancer cells via binding pneumococcal surface protein C (PspC) to platelet-activating factor receptor (PAFR). Interaction between PspC and PAFR stimulates cell proliferation and activates PI3K/AKT and nuclear factor kB (NF-kB) signaling pathways, which trigger a pro-inflammatory response. Lung cancer cells infected with SP form larger tumors in BALB/C mice compared to untreated cells. Mice treated with tobacco carcinogen and SP develop more lung tumors and had shorter survival period than mice treated with the carcinogen alone. Mutating PspC or PAFR abolishes tumor-promoting effects of SP. Overabundance of SP is associated with the survival. SP may play a driving role in lung tumorigenesis by activating PI3K/AKT and NF-kB pathways via binding PspC to PAFR and provide a microbial target for diagnosis and treatment of the disease. |
| first_indexed | 2024-04-10T09:32:05Z |
| format | Article |
| id | doaj.art-8789b7b4553c495d976511e70a6e4052 |
| institution | Directory Open Access Journal |
| issn | 2589-0042 |
| language | English |
| last_indexed | 2024-04-10T09:32:05Z |
| publishDate | 2023-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | iScience |
| spelling | doaj.art-8789b7b4553c495d976511e70a6e40522023-02-19T04:26:33ZengElsevieriScience2589-00422023-02-01262105923Streptococcus pneumoniae promotes lung cancer development and progressionNing Li0Huifen Zhou1Van K. Holden2Janaki Deepak3Pushpa Dhilipkannah4Nevins W. Todd5Sanford A. Stass6Feng Jiang7Department of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA; Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USADepartment of Pathology, University of Maryland School of Medicine, Baltimore, MD, USADepartment of Medicine, University of Maryland School of Medicine, Baltimore, MD, USADepartment of Medicine, University of Maryland School of Medicine, Baltimore, MD, USADepartment of Pathology, University of Maryland School of Medicine, Baltimore, MD, USADepartment of Medicine, University of Maryland School of Medicine, Baltimore, MD, USADepartment of Pathology, University of Maryland School of Medicine, Baltimore, MD, USADepartment of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA; Corresponding authorSummary: Streptococcus pneumoniae (SP) is associated with lung cancer, yet its role in the tumorigenesis remains uncertain. Herein we find that SP attaches to lung cancer cells via binding pneumococcal surface protein C (PspC) to platelet-activating factor receptor (PAFR). Interaction between PspC and PAFR stimulates cell proliferation and activates PI3K/AKT and nuclear factor kB (NF-kB) signaling pathways, which trigger a pro-inflammatory response. Lung cancer cells infected with SP form larger tumors in BALB/C mice compared to untreated cells. Mice treated with tobacco carcinogen and SP develop more lung tumors and had shorter survival period than mice treated with the carcinogen alone. Mutating PspC or PAFR abolishes tumor-promoting effects of SP. Overabundance of SP is associated with the survival. SP may play a driving role in lung tumorigenesis by activating PI3K/AKT and NF-kB pathways via binding PspC to PAFR and provide a microbial target for diagnosis and treatment of the disease.http://www.sciencedirect.com/science/article/pii/S2589004222021964BacteriologyCell biologyCellCancer systems biology |
| spellingShingle | Ning Li Huifen Zhou Van K. Holden Janaki Deepak Pushpa Dhilipkannah Nevins W. Todd Sanford A. Stass Feng Jiang Streptococcus pneumoniae promotes lung cancer development and progression iScience Bacteriology Cell biology Cell Cancer systems biology |
| title | Streptococcus pneumoniae promotes lung cancer development and progression |
| title_full | Streptococcus pneumoniae promotes lung cancer development and progression |
| title_fullStr | Streptococcus pneumoniae promotes lung cancer development and progression |
| title_full_unstemmed | Streptococcus pneumoniae promotes lung cancer development and progression |
| title_short | Streptococcus pneumoniae promotes lung cancer development and progression |
| title_sort | streptococcus pneumoniae promotes lung cancer development and progression |
| topic | Bacteriology Cell biology Cell Cancer systems biology |
| url | http://www.sciencedirect.com/science/article/pii/S2589004222021964 |
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