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Previous studies have shown the role of bacterial lipopolysaccharide (LPS) in promoting tumor progression. Our previous study found that the community richness of LPS-producing bacteria was significantly increased in the fresh stool samples of esophageal cancer (EC) patients, but the relative LPS levels and underlying mechanism in EC progression remain unknown. In this study, an case-control study found that the content of LPS was higher in serum of EC patients. Functional experiments of CCK8 assay and transwell assay showed that LPS contributed to the proliferation, migration, invasion of EC109 cells. Meanwhile, LPS induced EC109 to secrete IL-6 and TGF-β1. Western blot analysis revealed the level of TLR4 and NF-κB increased significantly after LPS treatment. Epithelial marker Ecadherin was significantly down-regulated and interstitial marker N-cadherin and Vimentin were up-regulated after LPS treatment. However, TAK242 (TLR4 inhibitor) or PDTC (NF-κB inhibitor) could eliminate the inflammatory and EMTpromoting effects of LPS. In total, our results suggested that LPS exacerbated to the migration, invasion, and epithelial-mesenchymal transition of EC109 cells by TLR4/NF-κB axis. High level LPS may have a critical effect on the occurrence and development of EC.

Background The effects of e-cigarettes on endothelial function remained controversial. Aim The study aimed to investigate the effects of e-cigarettes on vascular endothelial function. Methods PubMed, Web of Science, Embase, and Cochrane Library were searched up to December 2021. We only included the studies in which the control group included vaping without nicotine and tobacco. Pairwise and network meta-analyses were conducted for flow-mediated dilation (FMD), pulse wave velocity (PWV), and heart rate corrected augmentation index (AIx75). Results Eight studies involving 372 participants were eligible for this review. Compared with vaping without nicotine, e-cigarettes significantly increase in PWV (Mean difference = 3.09; 95% Confidential Interval: 1.51 to 4.68, p < 0.001) and AIx75 (Mean difference = 2.11; 95% Confidential Interval: 1.02 to 3.21, p < 0.001) indicators, but not affect FMD (Mean difference = 0.78; 95% Confidential Interval: -0.08 to 1.64, p = 0.075). But compared with traditional tobacco, e-cigarettes did not affect FMD (Mean difference = 0.28, 95% Confidential Interval: -0.45 to 0.59, p = 0.084). According to SUCRA, The e-cigarette ranked first for FMD (SUCRA = 97%), tobacco ranked first for PWV (SUCRA = 75%), and AIX75(SUCRA = 99%). Conclusions In summary, evidence from our pooled analyses indicated that acute inhalation of e-cigarettes leads to negative changes in vascular endothelial function. E-cigarettes cannot be used as an alternative to public health strategies for tobacco control and should not be considered cardiovascular safety products. More future research should be conducted to verify our findings.

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