Atrazine’s path to cancer possibly clarified

Scientists have identified a cellular button that the controversial herbicide presses to promote tumor development


WEEDWACKER  One of the most common herbicides used on crops in the United States may help sow cancer cells.

Lars Ploughmann/flickr (CC BY-SA 2.0)

A controversial weed killer may inadvertently act as a fertilizer for human cancer cells — and scientists are closer to understanding how.

Researchers have pinpointed the cellular pathway that allows the herbicide atrazine to mimic estrogen and fire up cancer cells, according to a study published January 16 in Environmental Health Perspectives.

Atrazine, an herbicide that can seep from crop fields and pollute drinking water, is known to disrupt hormone signaling in humans (SN: 2/27/10, p. 18). Exposure to atrazine has been linked to increased rates of ovarian and breast cancer. In 2004, the European Union banned the chemical, but atrazine is widely applied in the United States. 

Scientists have long suspected that atrazine acts as an estrogen doppelgänger in cells. But in a puzzling twist, researchers discovered that atrazine can’t rouse the main estrogen receptor. Through this receptor, the hormone — and presumably a mimic — sets off a response, gaining the power to turn on genes and control development of reproductive organs. Without such capabilities, atrazine’s hormonelike effects were surprising.

In the new study, researchers led by Marcello Maggiolini of the University of Calabria in Rende, Italy, found that atrazine binds to a different estrogen receptor, called GPER. They discovered that atrazine roused GPER in breast and ovarian cancer cells. The study also showed that the estrogen impostor spurred ovarian cancer cells to multiply.

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