Mechanistically, we found that Escherichia-Shigella- and unclassified_f__Enterobacteriaceae-derived LPS activated the TLR4-mTOR-NF-κB-IL-6 axis to facilitate NSCLC cell proliferation, whereas rapamycin effectively delayed LPS-induced tumor cell proliferation in vitro and in vivo functional experiments. This evidence concerns the gene TLR4 and non-small cell lung carcinoma.