2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces matrix metalloproteinase (MMP) expression and invasion in A2058 melanoma cells

Villano, Caren M.; Murphy, Kyle; Akintobi, A.; White, Lori A.

doi:10.1016/j.taap.2005.05.001

Cited by 95 publications

(65 citation statements)

References 50 publications

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“…FLS-RA have also shown the ability to invade normal human cartilage engrafted in SCID mice (Muller-Ladner et al, 1996). Activation of the AHR pathway by an exogenous ligand like TCDD in lung airway epithelial cells, normal human keratinocytes and melanocytes, and the melanoma cell line A2058 induces expression of MMP-2 and -9 (Martinez et al, 2002;Villano et al, 2006). Our data show in RA-FLS that IL1B induced MMP-2 and MMP-9 (gelatinase A and B) mRNA expression; however, this induction was significantly attenuated by GNF351 treatment.…”

Section: Ah Receptor Stimulates Growth Factor Expressionmentioning

confidence: 56%

Aryl Hydrocarbon Receptor Antagonism Attenuates Growth Factor Expression, Proliferation, and Migration in Fibroblast-Like Synoviocytes from Patients with Rheumatoid Arthritis

Lahoti

Hughes

Kusnadi

et al. 2013

J Pharmacol Exp Ther

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Rheumatoid arthritis (RA) is a chronic autoimmune disease with high morbidity and mortality. Within the inflammatory milieu, resident fibroblast-like synoviocytes (FLS) in the synovial tissue undergo hyperplasia, which leads to joint destruction. Epidemiologic studies and our previous research suggest that activation of the aryl hydrocarbon receptor (AHR) pathway plays an instrumental role in the inflammatory and destructive RA phenotype. In addition, our recent studies implicate the AHR in the regulation of the expression of several growth factors in established tumor cell lines. Thus, under inflammatory conditions, we hypothesized that the AHR is involved in the constitutive and inducible expression of several growth factors, FLS proliferation and migration, along with protease-dependent invasion in FLS from patients with RA

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Section: Ah Receptor Stimulates Growth Factor Expressionmentioning

confidence: 56%

Aryl Hydrocarbon Receptor Antagonism Attenuates Growth Factor Expression, Proliferation, and Migration in Fibroblast-Like Synoviocytes from Patients with Rheumatoid Arthritis

Lahoti

Hughes

Kusnadi

et al. 2013

J Pharmacol Exp Ther

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“…Aryl hydrocarbons such as TCDD and benzo(a)pyrene induced the expression of MMP-9 in PC-3 and DU145 human prostrate cancer cells (Haque et al, 2005). TCDD increased the expression and activity of MMP-1, MMP-2, and MMP-9 in transformed melanoma cell (A2058) and increased invasion (Villano et al, 2006). Gene expression in the fetal murine heart after TCDD exposure in utero suggests possible alterations in cell-cycle control and ECM production and remodeling (Thackaberry et al, 2005).…”

Section: Downloaded Frommentioning

confidence: 99%

Aryl Hydrocarbon Receptor Activation Inhibits Regenerative Growth

2005

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There is considerable literature supporting the conclusion that inappropriate activation of the aryl hydrocarbon receptor (AHR) alters cellular signaling. We have established previously that fin regeneration is specifically inhibited by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in adult zebrafish and have used this in vivo endpoint to evaluate interactions between AHR and growth-controlling pathways. Because there are experimental limitations in studying regeneration in adult animals, we have developed a larval model to evaluate the effect of AHR activation on tissue regeneration. Two-day-old zebrafish regenerate their amputated caudal fins within 3 days. Here, we demonstrate that TCDD specifically blocks regenerative growth in larvae. The AHR pathway in zebrafish is considerably more complex than in mammals, with at least three zebrafish AHR genes (zfAHR1a, zfAHR1b, and zfAHR2) and two ARNT genes (zfARNT1 and zfARNT2). Although it was presumed that the block in regeneration was mediated by AHR activation, it had not been experimentally demonstrated. Using antisense morpholinos and mutant fish lines, we report that zfAHR2 and zfARNT1 are the in vivo dimerization partners that are required for inhibition of regeneration by TCDD. Several pathways including fibroblast growth factor (FGF) signaling are essential for fin regeneration. Even though impaired FGF signaling and TCDD exposure both inhibit fin regeneration, their morphometric response is distinct, suggesting that the mechanisms of impairment are different. With the plethora of molecular and genetic techniques that can be applied to larval-stage embryos, this in vivo regeneration system can be further exploited to understand cross-talk between AHR and other signaling pathways.

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“…Interestingly, these levels corresponded to increasing invasiveness of melanoma cells but were lower than that seen in melanocytes. In the highly invasive A2058 melanoma cells, the expression of AhR target genes, CYP1A1 and CYP1B1 was increased by TCDD which is a known stimulator of this signalling pathway (Villano et al, 2006). The use of AhR antagonist abrogated CYP1 expression in A2058 cells which suggests that this signalling pathway is functional in these tumour cells.…”

Section: Aryl Hydrocarbon Receptormentioning

confidence: 94%

“…On the whole, there is evidence to suggest that melanocytes express functional AhR which can be activated by UV radiation (Jux et al, 2011;Luecke et al, 2010). Melanoma cells express AhR mRNA which corresponds to its intracellular protein content (Villano et al, 2006). Interestingly, these levels corresponded to increasing invasiveness of melanoma cells but were lower than that seen in melanocytes.…”

Section: Aryl Hydrocarbon Receptormentioning

confidence: 99%