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Pair of cancer genes found to drive both cell migration and division

he other side. But when both enzymes are missing, levels of PIP3 remain constant throughout the membrane, and the cell can't migrate properly.

In experiments with single-celled amoebae, Devreotes and his team learned that PTEN and PI3K do the same thing to PIP3 in dividing cells. When a normal cell prepares to divide, it first doubles its genetic material, and then creates a "furrow" down the middle, cutting the cell in half. The research team noticed that the two halves of a normal dividing cell looked and acted like two cells moving away from each other.

"Essentially, the two halves are like migrating cells - PIP3 levels are high on the sides that represent the 'fronts' of what will be two new cells, and they are low at the furrow, or what amounts to the back of the new cells," says Devreotes.

In their experiments, cells without PTEN and PI3K couldn't regulate levels of PIP3, and they divided much slower than normal cells. These cells became "stuck" and accumulated many copies of their genetic material because they could do everything required for cell division except complete the split, the researchers found.

"There are ways the cell can make PIP3 even when PI3K is missing, but the major way to break it down is by using PTEN. So if PTEN isn't there to destroy PIP3 at the furrow, the halves can't pull apart," says Chris Janetopoulos, Ph.D., a research associate in Devreotes's lab and first author on the paper. The cells' problems were eliminated when the researchers added the human PTEN gene to the mutated amoebae. Like the amoeba's own PTEN, the human version cleaned up PIP3, restoring its normal distribution within the cell. This indicates that human cells likely use the new mechanism to divide as well.

The next steps are to study the roles of the two genes in dividing cells by seeing if controlling the location of the PTEN and PI3K proteins can determine the direction in which cells divide, Devreotes says.


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Source:Johns Hopkins Medical Institutions


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