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

Gonçalves, Márcia; Cappellari, Angélica Regina; Santos, André A.; Macchi, Fernanda Souza; Antunes, Krist Helen; Souza, Ana Paula Duarte de; Morrone, Fernanda Bueno

doi:10.1590/1678-4324-2016150485

Cited by 14 publications

(10 citation statements)

References 54 publications

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“…This observation is not always in agreement with the previous reports. Thus, P. gingivalis LPS, at concentrations similar to that used in our study, enhanced the proliferation/viability of primary human oral epithelial cells [ 43 ], but did not affect that of oral squamous carcinoma cells [ 44 ]. TNF-α at a concentration of 100 ng/mL was shown to induce the apoptosis of primary gingival epithelial cells [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study

Holl

Wang

et al. 2021

IJERPH

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Smoking is a well-recognized risk factor for oral mucosal and periodontal diseases. Nicotine is an important component of cigarette smoke. This study aims to investigate the impact of nicotine on the viability and inflammatory mediator production of an oral epithelial cell line in the presence of various inflammatory stimuli. Oral epithelial HSC-2 cells were challenged with nicotine (10−8–10−2 M) for 24 h in the presence or absence of Porphyromonas gingivalis lipopolysaccharide (LPS, 1 µg/mL) or tumor necrosis factor (TNF)-α (10−7 M) for 24 h. The cell proliferation/viability was determined by MTT assay. Gene expression of interleukin (IL)-8, intercellular adhesion molecule (ICAM)-1, and β-defensin was assayed by qPCR. The production of IL-8 protein and cell surface expression of ICAM-1 was assessed by ELISA and flow cytometry, respectively. Proliferation/viability of HSC-2 cells was unaffected by nicotine at concentrations up to 10−3 M and inhibited at 10−2 M. Nicotine had no significant effect on the basal expression of IL-8, ICAM-1, and β-defensin. At the same time, it significantly diminished P. gingivalis LPS or the TNF-α-induced expression levels of these factors. Within the limitations of this study, the first evidence was provided in vitro that nicotine probably exerts a suppressive effect on the production of inflammatory mediators and antimicrobial peptides in human oral epithelial cells.

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Section: Discussionmentioning

confidence: 99%

Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study

Holl

Wang

et al. 2021

IJERPH

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“…LPS is found in the cell wall of Gram-negative bacteria. Previous studies have shown that P. gingivalis LPS tend to increase the viability of oral cancer cells [3]. Studies of the tumour microenvironment have shown that macrophages demonstrate increased IL-6 and CD14 expression and increased nitric oxide secretion after the stimulation of LPS [2].…”

Section: Introductionmentioning

confidence: 99%

Bacterial Antigens Reduced the Inhibition Effect of Capsaicin on Cal 27 Oral Cancer Cell Proliferation

Chakraborty

Vickery

Darido

et al. 2021

IJMS

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Oral cancer is a major global health problem with high incidence and low survival rates. The oral cavity contains biofilms as dental plaques that harbour both Gram-negative and Gram-positive bacterial antigens, lipopolysaccharide (LPS) and lipoteichoic acid (LTA), respectively. LPS and LTA are known to stimulate cancer cell growth, and the bioactive phytochemical capsaicin has been reported to reverse this effect. Here, we tested the efficacy of oral cancer chemotherapy treatment with capsaicin in the presence of LPS, LTA or the combination of both antigens. LPS and LTA were administered to Cal 27 oral cancer cells prior to and/or concurrently with capsaicin, and the treatment efficacy was evaluated by measuring cell proliferation and apoptotic cell death. We found that while capsaicin inhibits oral cancer cell proliferation and metabolism (MT Glo assay) and increases cell death (Trypan blue exclusion assay and Caspase 3/7 expression), its anti-cancer effect was significantly reduced on cells that are either primed or exposed to the bacterial antigens. Capsaicin treatment significantly increased oral cancer cells’ suppressor of cytokine signalling 3 gene expression. This increase was reversed in the presence of bacterial antigens during treatment. Our data establish a rationale for clinical consideration of bacterial antigens that may interfere with the treatment efficacy of oral cancer.

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“…LPS treatment induces Ca 2+ entry in cancer cells in a TLR4-dependent manner, resulting in a chronic elevation of basal intracellular calcium levels [7]. Previous studies have shown that Porphyromonas gingivalis LPS tend to increase the viability of oral cancer cells [8], while within the tumour microenvironment, macrophage expression of IL-6 and CD14 is increased as well as free radical secretion [7]. Bacterial infection has been shown to be associated with chronic inflammation, anti-apoptotic activity, and pro-proliferative activities [9].…”

Section: Introductionmentioning

confidence: 99%

ML218 HCl Is More Efficient Than Capsaicin in Inhibiting Bacterial Antigen-Induced Cal 27 Oral Cancer Cell Proliferation

Chakraborty

Darido

et al. 2021

IJMS

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The bacterial antigen, lipopolysaccharide (LPS) and disruptions in calcium channels are independently known to influence oral cancer progression. Previously, we found that bacterial antigens, LPS and lipoteichoic acid (LTA) act as confounders during the action of capsaicin on Cal 27 oral cancer proliferation. As calcium channel drugs may affect oral cancer cell proliferation, we investigated the effect of ML218 HCl, a T-type voltage-gated calcium channel blocker, on the proliferation of Cal 27 oral cancer cells. We hypothesized that ML218 HCl could effectively reduce LPS-induced oral cancer cell proliferation. LPS and LTA antigens were added to Cal 27 oral cancer cells either prior to and/or concurrently with ML218 HCl treatment, and the efficacy of the treatment was evaluated by measuring Cal 27 proliferation, cell death and apoptosis. ML218 HCl inhibited oral cancer cell proliferation, increased apoptosis and cell death, but their efficacy was significantly reduced in the presence of bacterial antigens. ML218 HCl proved more effective than capsaicin in reducing bacterial antigen-induced Cal 27 oral cancer cell proliferation. Our results also suggest an interplay of proliferation factors during the bacterial antigens and calcium channel drug interaction in Cal 27. Bacterial antigen reduction of drug efficacy should be considered for developing newer pharmacological agents or testing the efficacy of the existing oral cancer chemotherapeutic agents. Finally, voltage gated calcium channel drugs should be considered for future oral cancer research.

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

Cited by 14 publications

References 54 publications

Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study

Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study

Bacterial Antigens Reduced the Inhibition Effect of Capsaicin on Cal 27 Oral Cancer Cell Proliferation

ML218 HCl Is More Efficient Than Capsaicin in Inhibiting Bacterial Antigen-Induced Cal 27 Oral Cancer Cell Proliferation

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