Sodium salicylate inhibits TNF-α-induced NF-κB activation, cell migration, invasion and ICAM-1 expression in human melanoma cells

Katerinaki, Efthymia; Haycock, John W.; Lalla, Ravindra; Carlson, Kenneth E.; Yang, Yifan; Hill, Rebecca P.; Lorigan, Paul; MacNeil, Sheila

doi:10.1097/01.cmr.0000195698.58013.53

Cited by 26 publications

(24 citation statements)

References 44 publications

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“…In addition, the present study suggested that the NFκB inhibitor aspirin nearly blocked the TNF-α-induced EMT, suggesting that NFκB may be the converging point of the complicated signal pathway induced by TNF-α in the process of tumor metastasis. In agreement with previous study showing that inhibition of NFκB would significantly inhibit the migrating ability of tumor cells (24,25), our result may also provide valuable information for the role of aspirin in inflammation-associated tumors for the prevention of metastasis. However, it is important to note that aspirin is not a specific inhibitor of NFκB, but COX-2 is also blocked by aspirin which plays an important role in tumor metastasis.…”

Section: Discussionsupporting

confidence: 92%

Role of nuclear factor kappa B and reactive oxygen species in the tumor necrosis factor-a-induced epithelial-mesenchymal transition of MCF-7 cells

Dong

Wang

et al. 2007

Braz J Med Biol Res

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The microenvironment of the tumor plays an important role in facilitating cancer progression and activating dormant cancer cells. Most tumors are infiltrated with inflammatory cells which secrete cytokines such as tumor necrosis factor-α (TNF-α). To evaluate the role of TNF-α in the development of cancer we studied its effects on cell migration with a migration assay. The migrating cell number in TNF-α-treated group is about 2-fold of that of the control group. Accordingly, the expression of E-cadherin was decreased and the expression of vimentin was increased upon TNF-α treatment. These results showed that TNF-α can promote epithelial-mesenchymal transition (EMT) of MCF-7 cells. Further, we found that the expression of Snail, an important transcription factor in EMT, was increased in this process, which is inhibited by the nuclear factor kappa B (NFκB) inhibitor aspirin while not affected by the reactive oxygen species (ROS) scavenger N-acetyl cysteine. Consistently, specific inhibition of NFκB by the mutant IκBα also blocked the TNF-α-induced upregulation of Snail promoter activity. Thus, the activation of NFκB, which causes an increase in the expression of the transcription factor Snail is essential in the TNF-α-induced EMT. ROS caused by TNF-α seemed to play a minor role in the TNF-α-induced EMT of MCF-7 cells, though ROS per se can promote EMT. These findings suggest that different mechanisms might be responsible for TNF-α-and ROSinduced EMT, indicating the need for different strategies for the prevention of tumor metastasis induced by different stimuli. Correspondence

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Section: Discussionsupporting

confidence: 92%

Role of nuclear factor kappa B and reactive oxygen species in the tumor necrosis factor-a-induced epithelial-mesenchymal transition of MCF-7 cells

Dong

Wang

et al. 2007

Braz J Med Biol Res

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“…When compared to individual migration, collective migration, as in melanomas, presents higher dependence on cell-ECM adhesion [11]. In accordance with this statement, studies have shown that the presence of TNF-increased melanoma cell migration [12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 57%

Mathematical Modeling of Melanoma Cell Migration with an Elastic Continuum Model for the Evaluation of the Influence of Tumor Necrosis Factor-Alpha on Migration

Gallinaro

Marques

Azevedo

et al. 2013

Journal of Computational Medicine

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An elastic continuum mathematical model was implemented to study collective C8161 melanoma cell migration during a "scratch wound" assay, in control and under the influence of the proinflammatory cytokine tumour necrosis factor-alpha (TNF-). The model has four constants: force that results from lamellipod formation (F), adhesion constant between cells and extracellular matrix (ECM) (b), cell layer elasticity modulus (k), and growth rate ( ). A nonlinear regression routine was used to obtain the parameters of the model with data from an experiment made with C8161 melanoma cells, with and without TNF-. Coefficient of determination for both situations was 2 = 0.89 and 2 = 0.92, respectively. The parameters values obtained were similar to the ones found in the literature. However, the adhesion constant value decreased with the introduction of TNF-, which is not in accordance with expected since the presence of TNF-is associated with an increased expression of integrins that would promote an enhanced adhesion among cells. The model was used in a study relating to the adhesion constant and cell migration, and the results suggested that cell migration decreases with higher adhesion, which is also not in accordance with expected. These differences would not occur if it was considered that TNF-increases the elasticity modulus of the cell layer.

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“…22 Cells that had invaded the lower surface of the Matrigel-coated membrane were fixed onto a glass slide, stained using the Diff-Quik Stain set (Dade Behring, Newark, Del), and examined using light microscopy. The number of invading cells was scored by 2 independent observers.…”

Section: Transwell Invasion Assaymentioning

confidence: 99%

“…22 We used UT-SCC-74A and UT-SCC-90A (expressing high CLDN1 levels: 1846-fold and 1622-fold, respectively, compared with the normal fibroblast cell line Hs21Fs, expression 5 1) and UT-SCC-24A (expressing moderate levels: 292-fold). Relative CLDN1 levels in these lines were confirmed using a keratinocyte line derived from normal foreskin preparations (CLDN1 expression 5 7.68 compared with Hs21Fs; relative expression data for the UT-SCC lines was consistent irrespective of the normal control used).…”

Section: Cldn1 Overexpression and Invasion Of Oral Carcinoma Cellsmentioning

confidence: 99%

Claudin 1 overexpression increases invasion and is associated with aggressive histological features in oral squamous cell carcinoma

Reis

Bharadwaj

Machado

et al. 2008

Cancer

101

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BACKGROUND.The authors have previously shown that overexpression of claudin 1 (CLDN1) is associated with advanced disease stage in oral squamous cell carcinomas (OSCCs). Their goal was to examine CLDN1 expression in a large series of primary OSCCs and to further investigate whether CLDN1 overexpression plays a role in invasion in OSCC.METHODS.CLDN1 gene expression levels were determined by quantitative real‐time reverse transcription polymerase chain reaction (QRT‐PCR) in 100 primary OSCCs. CLDN1 protein expression was examined by immunohistochemistry in 70 of 100 OSCCs. E‐Cadherin protein levels were also assessed in 58 OSCCs. The authors performed a transwell Matrigel invasion assay for assessment of the invasive potential of CLDN1 overexpressing oral carcinoma cells. Western blotting and QRT‐PCR were used to assess CLDN1 expression in transfected cells and controls.RESULTS.CLDN1 mRNA was increased (median = 18.5) in 79 of 100 OSCCs, compared with normal oral mucosa (expression = 1.0). CLDN1 overexpression was associated with angiolymphatic (P = .037) and perineural invasion (P = .051). CLDN1 was highly expressed in 48 of 70 (68%) OSCCs. E‐Cadherin was lost or underexpressed in 49 of 58 (84%) OSCCs. The invasion assay showed that cells overexpressing CLDN1 have increased invasive potential, whereas small interfering RNA–mediated depletion of CLDN1 decreased the invasive potential of cells.CONCLUSIONS.CLDN1 overexpression is associated with angiolymphatic and perineural invasion, consistent with aggressive tumor behavior. Overexpression of CLDN1 protein is associated with increased invasiveness of oral carcinoma cells. Cancer 2008. © 2008 American Cancer Society.

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Sodium salicylate inhibits TNF-α-induced NF-κB activation, cell migration, invasion and ICAM-1 expression in human melanoma cells

Cited by 26 publications

References 44 publications

Role of nuclear factor kappa B and reactive oxygen species in the tumor necrosis factor-a-induced epithelial-mesenchymal transition of MCF-7 cells

Role of nuclear factor kappa B and reactive oxygen species in the tumor necrosis factor-a-induced epithelial-mesenchymal transition of MCF-7 cells

Mathematical Modeling of Melanoma Cell Migration with an Elastic Continuum Model for the Evaluation of the Influence of Tumor Necrosis Factor-Alpha on Migration

Claudin 1 overexpression increases invasion and is associated with aggressive histological features in oral squamous cell carcinoma

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