This dual role complicates efforts to develop cancer drugs that target the protein, but may lead to new therapies for heart muscle damage.
The protein, MCL1, is currently the focus of widespread cancer drug development efforts.
MCL1 is best known as an inhibitor of death via the cell's suicide pathway in a process called apoptosis.
The protein is elevated in a variety of cancers, and a number of MCL1 inhibitors are in the cancer drug development pipeline worldwide.
The protein has also been linked to drug resistance in cancer patients. Until now, however, MCL1's role in heart muscle cells was unclear.
"Our study shows that MCL1 is required for normal cardiac function and that the protein may be critical in protecting the heart from apoptosis," Joseph Opferman, Ph.D., an associate member of the St. Jude Department of Biochemistry and the paper's corresponding author, said.
The results also have implications for treating heart muscle damage following heart attacks or other insults.
While limiting MCL1 in cancer cells might aid in destroying them, providing higher levels of the protein in heart muscle cells might benefit a patient recovering from a heart attack or other heart damage.
The research is published in the scientific journal Genes and Development.
Source-ANI
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