ArticleClinical & experimental metastasis2005
Benzo-[a]-pyrene increases invasion in MDA-MB-231 breast cancer cells via increased COX-II expression and prostaglandin E2 (PGE2) output.
Article in Clinical & experimental metastasis, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 52 citations in OpenAlex.
- Integrated network toxicology, molecular docking, and molecular dynamics simulation reveals mechanisms of benzo[a]pyrene-induced pan-cancer.BMC pharmacology & toxicology · 2026Article
- Article
- Environmental chemicals, breast cancer progression and drug resistance.Environmental health : a global access science source · 2020Review
- Critical Review on the Presence of Phthalates in Food and Evidence of Their Biological Impact.International journal of environmental research and public health · 2020Review
- Mechanistic evidence that benzo[a]pyrene promotes an inflammatory microenvironment that drives the metastatic potential of human mammary cells.Archives of toxicology · 2018Article
- Benzo(a)pyrene promotes Hep-G2 cell migration and invasion by upregulating phosphorylated extracellular signal-regulated kinase expression.Oncology letters · 2018Article
- Aryl Hydrocarbon Receptor Diet and Breast Cancer Risk.The Yale journal of biology and medicine · 2018Review
- The Complex Biology of the Aryl Hydrocarbon Receptor and Its Role in the Pituitary Gland.Hormones & cancer · 2017Review
- Cytoplasmic aryl hydrocarbon receptor regulates glycogen synthase kinase 3 beta, accelerates vimentin degradation, and suppresses epithelial-mesenchymal transition in non-small cell lung cancer cells.Archives of toxicology · 2017Article
- Effects of the lifestyle habits in breast cancer transcriptional regulation.Cancer cell international · 2016Review
- The impact of low-dose carcinogens and environmental disruptors on tissue invasion and metastasis.Carcinogenesis · 2015Review
- Endocrine disruption of the epigenome: a breast cancer link.Endocrine-related cancer · 2014Review
- The aryl hydrocarbon receptor directs hematopoietic progenitor cell expansion and differentiation.Blood · 2013Article
- Ah receptor antagonism represses head and neck tumor cell aggressive phenotype.Molecular cancer research : MCR · 2012Article
- The novel lupus antigen related protein acheron enhances the development of human breast cancer.International journal of cancer · 2012Article
- Prenatal environmental exposures, epigenetics, and disease.Reproductive toxicology (Elmsford, N.Y.) · 2011Review
- Ah receptor antagonism inhibits constitutive and cytokine inducible IL6 production in head and neck tumor cell lines.Molecular carcinogenesis · 2011Article
- Epigenetic effects and molecular mechanisms of tumorigenesis induced by cigarette smoke: an overview.Journal of oncology · 2011Article
- Regulation of constitutive and inducible AHR signaling: complex interactions involving the AHR repressor.Biochemical pharmacology · 2009Review
- Targeting of aryl hydrocarbon receptor-mediated activation of cyclooxygenase-2 expression by the indole-3-carbinol metabolite 3,3'-diindolylmethane in breast cancer cells.The Journal of nutrition · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Benzo-[a]-pyrene (B[a]P), a carcinogenic component of cigarette smoke, has been shown to increase both COX-II expression and prostaglandin output in vascular smooth muscle and oral epithelial cells. In addition, invasive breast cancer cells have been reported to over express COX-II and PGE(2). Therefore, the objective of this study was to quantify the effect of increasing B[a]P concentrations on COX-II expression, PGE(2) output, and invasion using MDA-MB-231 cells, an invasive estrogen unresponsive breast cancer cell line. B[a]P significantly increased invasion in MDA-MB-231 cells at concentrations greater than 4 x 10(-8) M. Treatment of MDA-MB-231 cells with Vomitoxin (a selective COX-II inducer) enhanced invasion whereas co-treatment with NS398 (a selective COX-II inhibitor) attenuated B[a]P-induced invasion in MDA-MB-231 cells. Immunohistochemical staining and Western blots demonstrated a significant B[a]P treatment-induced increase in both the number of COX-II immunopositive MDA-MB-231 cells and COX-II protein levels. Moreover, B[a]P-treatment induced a profound (46 fold) increase in PGE(2) production by MDA-MB-231 cells. The aryl hydrocarbon receptor (AhR) antagonists resveratrol (RES) and alpha-naphthaflavone (alpha-NF) had no effect on their own, whereas B[a]P-induced invasion was significantly inhibited by co-treatment with RES and alpha-NF. Our data demonstrate that B[a]P-induced changes in invasion are mediated through augmented COX-II expression and PGE(2) production involving an AhR regulated pathway. Moreover, these results suggest a potential role for the AhR signalling pathway in breast cancer invasion.
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