Cold Spring Harbor scientists discover protein driver of prostate, lung cancer

Lung X-ray
New research from Cold Spring Harbor Laboratory fingers a protein deficiency that may drive one-third of lung tumors.

PTEN is often called an “anticancer” protein, because it prevents tumor cells from growing out of control. Mutations in the gene that encodes PTEN are commonly found in prostate cancer, lung cancer and other tumor types. But some patients with abnormally low levels of PTEN don’t carry any mutations in that gene—raising the question of what may be causing the protective protein to break down in those people.

Scientists at Cold Spring Harbor Laboratory have published research describing how another protein may help solve that conundrum. The protein is called Importin-11, and it normally protects PTEN by shuttling it into the nucleus of cells. When levels of Importin-11 diminish, PTEN degrades, leading to the development of cancer, the Cold Spring scientists reported in the Journal of Cell Biology.

"Our results suggest that Importin-11 is the 'Achilles' heel' of the … system that maintains the correct levels of PTEN inside cells," said Lloyd Trotman, professor at Cold Spring, in a press release.


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The gene that governs the protection of Importin-11 can also become mutated, and Trotman and his colleagues observed that lung cancer patients lacking that protein also have low levels of PTEN. They estimate that a loss of Importin-11 accounts for PTEN deficiencies in about a third of lung cancer patients.

Protecting PTEN is the focus of several oncology researchers looking for new approaches to tough-to-beat cancers. Last June, scientists at Ohio State University, for example, discovered that an enzyme called PRMT5 reduced PTEN levels in cells taken from patients with glioblastoma. Research at the University of Texas MD Anderson Cancer Center has also linked the loss of PTEN expression with cancer metastasis in the brain.

The Cold Spring Harbor team was able to show that several proteins in the cell cytoplasm work together to “tag” PTEN for destruction. So when Importin-11 escorts PTEN into the nucleus, it is in essence rescuing the tumor-suppressing protein by breaking up the cell machinery that’s designed to thwart it.

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