title: Glyphosate induces human breast cancer cells growth via estrogen receptors.
abstract: Glyphosate is an active ingredient of the most widely used herbicide and it is believed to be less toxic than other pesticides. However, several recent studies showed its potential adverse health effects to humans as it may be an endocrine disruptor. This study focuses on the effects of pure glyphosate on estrogen receptors (ERs) mediated transcriptional activity and their expressions. Glyphosate exerted proliferative effects only in human hormone-dependent breast cancer, T47D cells, but not in hormone-independent breast cancer, MDA-MB231 cells, at 10⁻¹² to 10⁻⁶M in estrogen withdrawal condition. The proliferative concentrations of glyphosate that induced the activation of estrogen response element (ERE) transcription activity were 5-13 fold of control in T47D-KBluc cells and this activation was inhibited by an estrogen antagonist, ICI 182780, indicating that the estrogenic activity of glyphosate was mediated via ERs. Furthermore, glyphosate also altered both ERα and β expression. These results indicated that low and environmentally relevant concentrations of glyphosate possessed estrogenic activity. Glyphosate-based herbicides are widely used for soybean cultivation, and our results also found that there was an additive estrogenic effect between glyphosate and genistein, a phytoestrogen in soybeans. However, these additive effects of glyphosate contamination in soybeans need further animal study.
authors.affiliation: Environmental Toxicology Program, Chulabhorn Graduate Institute, Laksi, Bangkok 10210, Thailand.
authors.forename: Siriporn
authors.initials: S
authors.lastname: Thongprakaisang
authors.forename: Apinya
authors.initials: A
authors.lastname: Thiantanawat
authors.forename: Nuchanart
authors.initials: N
authors.lastname: Rangkadilok
authors.forename: Tawit
authors.initials: T
authors.lastname: Suriyo
authors.forename: Jutamaad
authors.initials: J
authors.lastname: Satayavivad
mesh_terms: D001943:Breast Neoplasms / Q000139:chemically induced* / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D004357:Drug Synergism; D052244:Endocrine Disruptors / Q000737:chemistry / Q000633:toxicity*; D004965:Estrogen Antagonists / Q000494:pharmacology; D047628:Estrogen Receptor alpha / Q000819:agonists* / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D047629:Estrogen Receptor beta / Q000819:agonists* / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D004967:Estrogens / Q000737:chemistry / Q000633:toxicity; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D017930:Genes, Reporter / Q000187:drug effects; D019833:Genistein / Q000494:pharmacology; D005998:Glycine / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors / Q000633:toxicity; D006540:Herbicides / Q000037:antagonists & inhibitors / Q000633:toxicity*; D006801:Humans; D009363:Neoplasm Proteins / Q000819:agonists* / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D009376:Neoplasms, Hormone-Dependent / Q000139:chemically induced / Q000378:metabolism; D020218:Response Elements / Q000187:drug effects; D015533:Transcriptional Activation / Q000187:drug effects; D000097797:Glyphosate
chemical_list: D052244:Endocrine Disruptors; D004965:Estrogen Antagonists; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D004967:Estrogens; D019833:Genistein; D005998:Glycine; D006540:Herbicides; D009363:Neoplasm Proteins; D000097797:Glyphosate; C506487:ESR1 protein, human
keywords: Estrogenic effect; Genistein; Glyphosate; Human breast cancer; T47D; T47D-KBluc