G-Protein–Coupled Receptor 30 and Estrogen Receptor-α Are Involved in the Proliferative Effects Induced by Atrazine in Ovarian Cancer Cells
2008

Atrazine and Its Effects on Ovarian Cancer Cells

publication 10 minutes Evidence: moderate

Author Information

Author(s): Lidia Albanito, Rosamaria Lappano, Antonio Madeo, Adele Chimento, Eric R. Prossnitz, Anna Rita Cappello, Vincenza Dolce, Sergio Abonante, Vincenzo Pezzi, Marcello Maggiolini

Primary Institution: Department of Pharmaco-Biology, University of Calabria, Rende, Italy

Hypothesis

Can atrazine signal through GPR30 to stimulate biological responses in ovarian cancer cells?

Conclusion

Atrazine stimulates the proliferation of ovarian cancer cells through the GPR30–EGFR pathway without activating the estrogen receptor.

Supporting Evidence

  • Atrazine does not activate the estrogen receptor in cancer cells.
  • Atrazine stimulates ERK phosphorylation in ovarian cancer cells.
  • Atrazine induces the expression of estrogen target genes.
  • The proliferation of ovarian cancer cells induced by atrazine requires GPR30 and ERα.

Takeaway

Atrazine, a common pesticide, can make certain cancer cells grow faster by using a different pathway than the usual estrogen receptor.

Methodology

The study used gene reporter assays, signaling inhibitors, and gene silencing to evaluate the effects of atrazine on ovarian cancer cells.

Limitations

The study primarily focused on specific cancer cell lines, which may not fully represent in vivo conditions.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1289/ehp.11297

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