Laccase treatment impairs bisphenol A-induced cancer cell proliferation affecting estrogen receptor α-dependent rapid signals

Alessandro Bolli, Paola Galluzzo, Paolo Ascenzi, Giovanna Del Pozzo, Immacolata Manco, Maria Teresa Vietri, Luigi Mita, Lucia Altucci, Damiano Gustavo Mita, Maria Marino

Research output: Contribution to journalArticlepeer-review

Abstract

A wide variety of environmental contaminants exert estrogenic actions in wildlife, laboratory animals, and in human beings through binding to nuclear estrogen receptors (ERs). Here, the mechanism(s) of bisphenol A (BPA) to induce cell proliferation and the occurrence of its bioremediation by treatment with laccase are reported. BPA, highly present in natural world and considered as a model of environmental estrogen action complexity, promotes human cancer cell proliferation via ERα-dependent signal transduction pathways. Similar to 17α-estradiol, BPA increases the phosphorylation of both extracellular regulated kinase and AKT. Specific inhibitors of these kinase completely block the BPA effect on cancer cell proliferation. Notably, high BPA concentrations (i.e., 0.1 and 1 mM) are cytotoxic even in ERα-devoid cancer cells, indicating that an ERα-independent mechanism participates to BPA-induced cytotoxicity. On the other hand, BPA oxidation by laccase impairs the binding of this environmental estrogen to ERα loosing at all ERα-dependent effect on cancer cell proliferation. Moreover, the laccase-catalyzed oxidation of BPA reduces the BPA cytotoxic effect. Thus, laccase appears to impair BPA action(s), representing an invaluable bioremediation enzyme.

Original languageEnglish
Pages (from-to)843-852
Number of pages10
JournalIUBMB Life
Volume60
Issue number12
DOIs
Publication statusPublished - 2008

Keywords

  • Bisphenol A
  • Cell proliferation
  • Endocrine disruptor
  • Estrogen receptor α
  • Laccase-catalyzed inactivation of bisphenol A

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Clinical Biochemistry
  • Molecular Biology
  • Genetics

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