Streptococcus pneumoniae promotes lung cancer development and progression.

is associated with lung cancer, yet its role in the tumorigenesis remains uncertain. Herein we find that 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 form larger tumors in BALB/C mice compared to untreated cells. Mice treated with tobacco carcinogen and 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 . Overabundance of is associated with the survival. 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.