Journal Article

Increased ErbB-2 Tyrosine Kinase Activity, MAPK Phosphorylation, and Cell Proliferation in the Prostate Cancer Cell Line LNCaP following Treatment by Select Pesticides

Daniel M. Tessier and Fumio Matsumura

in Toxicological Sciences

Volume 60, issue 1, pages 38-43
Published in print March 2001 | ISSN: 1096-6080
Published online March 2001 | e-ISSN: 1096-0929 | DOI: http://dx.doi.org/10.1093/toxsci/60.1.38
Increased ErbB-2 Tyrosine Kinase Activity, MAPK Phosphorylation, and Cell Proliferation in the Prostate Cancer Cell Line LNCaP following Treatment by Select Pesticides

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The oncogene erbB-2 codes for a receptor tyrosine kinase that functions as a key mitotic signal in a variety of cell types. Amplification or overexpression of erbB-2 occurs in many forms of cancer, such as of the breast, colon, and prostate, and is an indicator of poor prognosis in those diseases. In the human prostate cancer cell lines LNCaP and PC-3, erbB-2 kinase was activated by pesticides of different chemical classes: (1) the organochlorine insecticides β-hexa-chlorocyclohexane (β-HCH), o,p'-dichlorodiphenyltrichloroethane (o,p'-DDT), and heptachlor epoxide; (2) the pyrethroid insecticide trans-permethrin, and (3) the fungicide chlorothalonil. o,p'-DDT also causes phosphorylation of mitogen-activated protein kinase (MAPK) and cellular proliferation of the androgen-dependent LNCaP line. However, no proliferative effect was observed in the androgen-independent PC-3 line. The proliferative effect of o,p'-DDT in LNCaP could not be blocked by the androgen receptor antagonist p,p'-dichlorodiphenyldichloroethene (p,p'-DDE), indicating that this effect of o,p'-DDT does not occur through direct interaction with the androgen receptor. Together these data demonstrate a putative mechanism for the action of certain pesticides in hormonal carcinogenesis.

Keywords: erbB-2/neu/HER-2; LNCaP; mitogen-activated protein kinase (MAPK); pesticides; prostate cancer; tyrosine kinases

Journal Article.  3994 words.  Illustrated.

Subjects: Medical Toxicology ; Toxicology (Non-medical)

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