Toll-Like Receptor-4 Is a Mediator of Proliferation in Esophageal Adenocarcinoma

Kohtz, Patrick D.; Halpern, Alison L.; Eldeiry, Mohamed; Hazel, Kweku; Kalatardi, Shana; Ao, Lihua; Meng, Xianzhong; Reece, T. Brett; Fullerton, David A.; Weyant, Michael J.

doi:10.1016/j.athoracsur.2018.08.014

Cited by 30 publications

(20 citation statements)

References 28 publications

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“…Dysregulation of TLR signaling within the gastrointestinal tract has been associated with cancer development (8)(9)(10). Additionally, previous work by our group has demonstrated a potential role of TLRs in the development and progression of esophageal adenocarcinoma (11,12).…”

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confidence: 79%

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Activation of Toll-Like Receptor 2 Promotes Proliferation of Human Lung Adenocarcinoma Cells

et al. 2020

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Background/Aim: The aim of this study was to evaluate the role of toll-like receptor 2 (TLR2) in the proliferation of human lung cancer cells and identify the signaling pathway that mediates this effect. Materials and Methods: Adenocarcinoma (A549 and H1650) and adenosquamous (H125) cells were treated with increasing doses of Pam3CSK4, a TLR2 agonist. Cell proliferation and NF-ĸB activation were evaluated. NF-ĸB was inhibited prior to treatment with Pam3CSK4 and proliferation was assessed. Results: TLR2 expression was significantly higher in A549 and H1650 cells compared to H125 cells (p<0.001). TLR2 stimulation induced proliferation in adenocarcinoma cells only and led to a corresponding increase in NF-ĸB activity (p<0.05). Inhibition of NF-ĸB prior to treatment with Pam3CSK4 attenuated this proliferative response. Conclusion: TLR2 activation induced proliferation of lung adenocarcinoma cells through activation of NF-ĸB. Thus, the TLR2 signaling pathway may be a potential therapeutic target in lung adenocarcinoma.

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confidence: 79%

“…This technique was adapted from previously published studies (11,19,20). Following cell treatments, cells were washed with PBS twice followed by lysis with 2x Laemmli Sample Buffer (Bio-Rad, Hercules, CA, USA) containing 5% 2mercaptoethanol.…”

Section: Western Blottingmentioning

confidence: 99%

Activation of Toll-Like Receptor 2 Promotes Proliferation of Human Lung Adenocarcinoma Cells

et al. 2020

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“…Other studies have found that baseline TLR4 expression is increased in esophageal adenocarcinoma cells compared with normal esophageal cells, and that stimulation with LPS results in intracellular MyD88/TRAF6/NF‐κB signaling and increased proliferation in all three cell lines tested. This proliferation was significantly reduced in the presence of the NF‐κB inhibitor Bay11‐7082 . Likewise, in HNSCC there is evidence that TLR4 intensity correlates with tumor grade, and that TLR4 activation promotes tumor development and protects the tumor from immune attack, suggesting that TLR4 engagement on tumor cells supports HNSCC progression …”

Section: Tlr4 In Head and Neck Squamous Cell Carcinomamentioning

confidence: 97%

“…This proliferation was significantly reduced in the presence of the NF-κB inhibitor Bay11-7082. 53 Likewise, in HNSCC there is evidence that TLR4 intensity correlates with tumor grade, and that TLR4 activation promotes tumor development and protects the tumor from immune attack, suggesting that TLR4 engagement on tumor cells supports HNSCC progression. 54…”

Section: Tlr4 In Head and Neck Squamous Cell Carcinomamentioning

confidence: 99%

TLR4 in skin cancer: From molecular mechanisms to clinical interventions

Dickinson

Wondrak

2019

Molecular Carcinogenesis

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The health and economic burden imposed by skin cancer is substantial, creating an urgent need for the development of improved molecular strategies for its prevention and treatment. Cutaneous exposure to solar ultraviolet (UV) radiation is a causative factor in skin carcinogenesis, and TLR4‐dependent inflammatory dysregulation is an emerging key mechanism underlying detrimental effects of acute and chronic UV exposure. Direct and indirect TLR4 activation, upstream of inflammatory signaling, is elicited by a variety of stimuli, including pathogen‐associated molecular patterns (such as lipopolysaccharide) and damage‐associated molecular patterns (such as HMGB1) that are formed upon exposure to environmental stressors, such as solar UV. TLR4 involvement has now been implicated in major types of skin malignancies, including nonmelanoma skin cancer, melanoma and Merkel cell carcinoma. Targeted molecular interventions that positively or negatively modulate TLR4 signaling have shown promise in translational, preclinical, and clinical investigations that may benefit skin cancer patients in the near future.

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“…The activation of TLR4 results in increased cell proliferation, which indicates an enhanced response in the process of inflammation-induced carcinogenesis. 113 In addition, microbes, e.g., Streptococcus pneumonia, may be associated with the upregulation of TLRs that mediate the molecular changes that occur in esophageal adenocarcinoma carcinogenesis under reflux conditions. 114 Reflux disease-related changes in IL-6 expression have been observed in several UAT tissues.…”

Section: Dysregulation Of the Mucosal Immune Systemmentioning

confidence: 99%

Laryngopharyngeal Reflux and Inflammatory Responses in Mucosal Barrier Dysfunction of the Upper Aerodigestive Tract

Liu¹,

Qian²,

Sun³

et al. 2021

JIR

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Toll-Like Receptor-4 Is a Mediator of Proliferation in Esophageal Adenocarcinoma

Cited by 30 publications

References 28 publications

Activation of Toll-Like Receptor 2 Promotes Proliferation of Human Lung Adenocarcinoma Cells

Activation of Toll-Like Receptor 2 Promotes Proliferation of Human Lung Adenocarcinoma Cells

TLR4 in skin cancer: From molecular mechanisms to clinical interventions

Laryngopharyngeal Reflux and Inflammatory Responses in Mucosal Barrier Dysfunction of the Upper Aerodigestive Tract

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