Abstract | BACKGROUND/AIM:
Perfluorooctanoic acid (PFOA) is one of the most common perfluorinated compounds widely used in several applications. Due to its persistence in the environment, PFOA has been associated with various diseases, including cancer. This study explored the effects of PFOA on follicular thyroid carcinoma cells (FTC133). MATERIALS AND METHODS: Cell invasion, migration, adhesion and activity of matrix metalloproteinase-2 (MMP-2) were investigated using Transwell assays, adhesion assay and gelatin zymography, respectively. The underlying mechanism involved in the effects observed was evaluated by immunoblot analyses. RESULTS: Treatment with PFOA did not affect cell migration, but enhanced cell invasion, adhesion and activity of MMP-2 in FTC133 cells. PFOA selectively enhanced the phosphorylation of nuclear factor kappa B (NF-κB) p65, as well as induced NF-κB nuclear translocation. Treatment with a NF-κB inhibitor (BAY 11-7085) was able to reverse PFOA-induced cell invasiveness. CONCLUSION: PFOA promotes invasiveness of FTC133 cells mediated through the activation of NF-κB signaling.
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Authors | Pipop Saejia, Kriengsak Lirdprapamongkol, Jisnuson Svasti, N Monique Paricharttanakul |
Journal | Anticancer research
(Anticancer Res)
Vol. 39
Issue 5
Pg. 2429-2435
(May 2019)
ISSN: 1791-7530 [Electronic] Greece |
PMID | 31092435
(Publication Type: Journal Article)
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Copyright | Copyright© 2019, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved. |
Chemical References |
- BAY 11-7085
- Caprylates
- Fluorocarbons
- NF-kappa B
- Nitriles
- RELA protein, human
- Sulfones
- Transcription Factor RelA
- perfluorooctanoic acid
- MMP2 protein, human
- Matrix Metalloproteinase 2
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Topics |
- Adenocarcinoma, Follicular
(drug therapy, genetics, pathology)
- Caprylates
(pharmacology)
- Cell Line, Tumor
- Cell Movement
(drug effects)
- Fluorocarbons
(pharmacology)
- Gene Expression Regulation, Neoplastic
(drug effects)
- Humans
- Matrix Metalloproteinase 2
(genetics)
- NF-kappa B
(antagonists & inhibitors, genetics)
- Neoplasm Invasiveness
(genetics, pathology)
- Nitriles
(pharmacology)
- Signal Transduction
(drug effects)
- Sulfones
(pharmacology)
- Transcription Factor RelA
(antagonists & inhibitors, genetics)
- Transcriptional Activation
(drug effects)
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