Lipopolysaccharide-induced toll-like receptor 4 signaling enhances the migratory ability of human esophageal cancer cells in a selectin-dependent manner

Effect of LPS on the Viability and Proliferation of Human Oral and Esophageal Cancer Cell Lines

“…Previous study has shown that LPS increases migration and adhesive properties of esophageal squamous carcinoma cells (HKESC-2 and HKESC-1) by TLR4 stimulation via p38 and selectin, contributing to tumor metastasis (Rousseau et al 2013). In fact, Rousseau et al (2013) tested a low LPS concentration of 0,1 µg/mL, and on this same concentration, we found that LPS increased tumor cells number. However, when we used higher concentrations of LPS we found a decrease in tumor cells number.…”

“…In macrophages, LPS induction actives transcription of genes encoding proinflammatory proteins, which leads to the release of cytokines and the synthesis of enzymes such as cyclooxygenase-2 (Niu et al 2015). Previous study has shown that LPS increases migration and adhesive properties of esophageal squamous carcinoma cells (HKESC-2 and HKESC-1) by TLR4 stimulation via p38 and selectin, contributing to tumor metastasis (Rousseau et al 2013). In fact, Rousseau et al (2013) tested a low LPS concentration of 0,1 µg/mL, and on this same concentration, we found that LPS increased tumor cells number.…”

“…TLR4 has been implicated in tumor cell invasion, survival, and metastasis in a variety of cancers (Yang et al 2014). Recent studies show that LPS can increase the migration ability of human cell esophageal cancer HKESC-2 by increasing its binding properties by signaling via TLR4 (Rousseau et al 2013). In this way, the aim of this study was to determine the action of LPS and PgLPS in cancer cell lines proliferation and viability using human esophagus OE19 and OE21 and the human oral carcinoma HN30.…”

Eritoran Suppresses Colon Cancer by Altering a Functional Balance in Toll-like Receptors That Bind Lipopolysaccharide

“…A previous study showed that the intrasplenic injection of eritoran in nude mice inhibited liver metastasis of colorectal cancer cells (54). Other studies in human colorectal and esophageal cancer cell lines have indicated that eritoran blocks LPS-induced TLR4 signaling for b1 integrin-and selectin-dependent cell adhesion and that it inhibits their migratory capability (54,55). Furthermore, eritoran has previously been shown to inhibit monocytic inflammatory responses in endotoxemic rats and virus-infected mice (22,29,30).…”

Re: Postoperative Complications do not Affect Long‐term Outcome in Esophageal Cancer Patients

“…This has been examined in a number of recent publications, many involving large-scale database analysis, across numerous specialties including operations for colorectal [2], lung [3], esophageal [4], gastric [5], and hepatic [6] malignancies. Though not yet fully elucidated, molecular and immune mechanisms underlying this relationship are being actively investigated; pathways including neutrophil-cancer cell interactions [7,8] and bacterial antigen receptor cell activation [9,10] have been previously implicated. A recent meta-analysis of long-term survival following complications after surgery published by our group [11], incorporating results for over 20,000 patients, has reported similar conclusions, with a significant reduction in long-term survival for patients with postoperative complications (hazard ratio and 95 % confidence interval: 1 Considering this discrepancy, we note that in Lindner and colleagues' examined cohort, adenocarcinoma patients who suffered major complications had a reduced survival (median 29.9 months) compared to those with no complications (33.2 months), with a similar trend for patients who suffered anastomotic leak (33.7 months) compared to those who did not (42.8 months).…”