Broccoli Compound Triggers the Function of Potent Tumor Suppressor

It turns out your mother was right. Broccoli and other cruciferous vegetables are good for you.
Loukia Papadopoulos

New research has pinpointed a compound in broccoli and other cruciferous vegetables that inactivates a gene known to play a crucial role in common cancers. The work may see the creation of new tumor-fighting compounds.


A new important player

"We found a new important player that drives a pathway critical to the development of cancer, an enzyme that can be inhibited with a natural compound found in broccoli and other cruciferous vegetables," said Pier Paolo Pandolfi, MD, PhD, Director of the Cancer Center and Cancer Research Institute at Beth Israel Deaconess Medical Center.

"This pathway emerges not only as a regulator for tumor growth control, but also as an Achilles' heel we can target with therapeutic options."

The key lies in a potent tumor suppressive gene called PTEN. Previous research has found that tumor cells exhibit lower levels of PTEN.

This has led scientists to debate whether restoring PTEN activity to normal levels in patients with cancer can unleash the gene's tumor suppressive properties. To figure this out, Pandolfi and his team identified the molecules and compounds regulating PTEN function and activation.

They found that a gene called WWP1 produces an enzyme that inhibits PTEN's tumor suppressive activity. They then were able to deduce that a small molecule, named indole-3-carbinol (I3C), could be the key to disabling the cancer causing effects of WWP1.

I3C and its effects

I3C is present in broccoli and its relatives and when administered to cancer-prone lab subjects it was found to inactivate WWP1. This then allowed PTEN to fully express its tumor suppressive powers.

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Unfortunately, the compound is found in such low amounts that the researchers say you would have to eat nearly 6 pounds of Brussels sprouts a day to reap its benefits. That's why Pandolfi and his team are now investigating better alternatives for the use of WWP1 that include developing more potent WWP1 inhibitors.

"Either genetic or pharmacological inactivation of WWP1 with either CRISPR technology or I3C could restore PTEN function and further unleash its tumor suppressive activity," said Pandolfi.

"These findings pave the way toward a long-sought tumor suppressor reactivation approach to cancer treatment." 

The study was published in the journal in Science.

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