Li Ning, Zhou Huifen, Holden Van K, Deepak Janaki, Dhilipkannah Pushpa, Todd Nevins W, Stass Sanford A, Jiang Feng
Department of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA.
Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
iScience. 2023 Jan 4;26(2):105923. doi: 10.1016/j.isci.2022.105923. eCollection 2023 Feb 17.
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.
与肺癌相关,但其在肿瘤发生中的作用仍不确定。在此我们发现,通过结合肺炎球菌表面蛋白C(PspC)与血小板活化因子受体(PAFR)附着于肺癌细胞。PspC与PAFR之间的相互作用刺激细胞增殖并激活PI3K/AKT和核因子κB(NF-κB)信号通路,从而引发促炎反应。与未处理的细胞相比,感染的肺癌细胞在BALB/C小鼠中形成更大的肿瘤。用烟草致癌物和处理的小鼠比单独用致癌物处理的小鼠发生更多的肺肿瘤且生存期更短。突变PspC或PAFR可消除的促肿瘤作用。的过量与生存相关。可能通过将PspC与PAFR结合激活PI3K/AKT和NF-κB通路在肺肿瘤发生中起驱动作用,并为该疾病的诊断和治疗提供微生物靶点。
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