Harnessing the survival powers of cancer cells could wipe out heart disease

A gene called Pim1 may give some kinds of cancer much of their potency, but it could also save your heart(Credit: Mark Sussman)

The same genes that allow many cancers to proliferate and thrive could in the future be repurposed as a force for good. A study at the San Diego State University (SDSU) Heart Institute has found that mouse hearts regenerate cells better, causing the mice to live longer, when their progenitor cells are modified to over-express a key gene in cancer production. The researchers believe this could lead to a new treatment for people with heart disease or who have suffered from other age-related cardiac problems.

The human heart normally heals and repairs itself using cardiac progenitor cells, which are basically cells that transform themselves into whatever specific type of heart cell is required. But as we get older, the process becomes less efficient. The body's self-therapy treatment weakens or stops entirely. This can lead to heart disease or cause complications in the recovery of people who have suffered heart failure.

Heart progenitor cells essentially wear out, and when they wear out they get cautious about dividing further to keep the supply up. Scientists believe they evolved to do this to protect the heart – if there's a transcription error during cell division, that could be it for you because even a minor problem in the heart can kill you.

The SDSU researchers think they can change this, however. The key is an enzyme called Pim, which is instrumental in the growth and proliferation of certain types of cancer cells but also in the division of healthy cells.

Pim is encoded by a gene called PIM1, which has been found to have no negative impact (i.e., it doesn't cause cancer) unless paired with another gene called Myc. Heart progenitor cells have nothing to do with Myc, so the researchers decided to modify them to over-express PIM1.

Their rodent trial was a huge success, with mouse progenitor cells given the PIM1 over-expression treatment in the nucleus dividing more prolifically, while cells modified in the mitochondria (the membrane that generates energy for the cell) lived longer because the enzyme inhibited their natural self-destruct signals.

The researchers found the same results when they tested heart tissue from people living on a ventricular assist device that pumps their blood for them (because their heart has failed).

They now hope to perform human clinical trials, with cardiac progenitor cells removed, modified to over-express PIM1, then returned to the patient's failing heart to see if it kicks the self-healing mechanisms back into life.

This is not the only research that could lead to self-repairing hearts. Earlier this month, researchers from the Temple University School of Medicine revealed promising early results with using stem cell exosomes (tiny sacks that act as messengers), and in particular a gene-regulating molecule from the exosomes, to augment the heart's self-repair capabilities. There was also talk a few years ago of a potential vaccine for heart disease, which would not induce self-healing so much as reduce the damage when self-healing starts to slow.

A paper describing the SDSU study was published in the Journal of Biological Chemistry.

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