Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Perfluorooctanoic acid (PFOA) exposure promotes proliferation, migration and invasion potential in human breast epithelial cells
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
2018 (English)In: Archives of Toxicology, ISSN 0340-5761, E-ISSN 1432-0738, Vol. 92, no 5, p. 1729-1739Article in journal (Refereed) Published
Abstract [en]

Despite significant advances in early detection and treatment, breast cancer remains a major cause of morbidity and mortality. Perfluorooctanoic acid (PFOA) is a suspected endocrine disruptor and a common environmental pollutant associated with various diseases including cancer. However, the effects of PFOA and its mechanisms of action on hormone-responsive cells remain unclear. Here, we explored the potential tumorigenic activity of PFOA (100 nM-1 mM) in human breast epithelial cells (MCF-10A). MCF-10A cells exposed to 50 and 100 mu M PFOA demonstrated a higher growth rate compared to controls. The compound promoted MCF-10A proliferation by accelerating G(0)/G(1) to S phase transition of the cell cycle. PFOA increased cyclin D1 and CDK4/6 levels, concomitant with a decrease in p27. In contrast to previous studies of perfluorooctane sulfate (PFOS), the estrogen receptor antagonist ICI 182,780 had no effect on PFOA-induced cell proliferation, whereas the PPAR alpha antagonist GW 6471 was able to prevent the MCF-10A proliferation, indicating that the underlying mechanisms involve PPAR alpha-dependent pathways. Interestingly, we also showed that PFOA is able to stimulate cell migration and invasion, demonstrating its potential to induce neoplastic transformation of human breast epithelial cells. These results suggest that more attention should be paid to the roles of PFOA in the development and progression of breast cancer.

Place, publisher, year, edition, pages
Springer Berlin/Heidelberg, 2018. Vol. 92, no 5, p. 1729-1739
Keywords [en]
Endocrine disrupting chemicals, EDCs, MCF-10A cells, Breast cancer, Cyclin D, P27
National Category
Pharmacology and Toxicology
Identifiers
URN: urn:nbn:se:uu:diva-357023DOI: 10.1007/s00204-018-2181-4ISI: 000432976700005PubMedID: 29502166OAI: oai:DiVA.org:uu-357023DiVA, id: diva2:1238004
Funder
Swedish Research Council FormasAvailable from: 2018-08-10 Created: 2018-08-10 Last updated: 2018-08-10Bibliographically approved

Open Access in DiVA

fulltext(1891 kB)3 downloads
File information
File name FULLTEXT01.pdfFile size 1891 kBChecksum SHA-512
e13b464081daa4c4d7e7a96f48f78e4c8202eb05162ef563012d8d36b04c4462c21210911fc2bbf6e9d6b3a0f0ad4f1655ad3da453c51f8799e39da368391ddc
Type fulltextMimetype application/pdf

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Pierozan, PaulaJernerén, FredrikKarlsson, Oskar
By organisation
Department of Pharmaceutical Biosciences
In the same journal
Archives of Toxicology
Pharmacology and Toxicology

Search outside of DiVA

GoogleGoogle Scholar
Total: 3 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 8 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf