A regulator called NIK, a protein that regulates immune cell function and inflammation, is also present on mitochondria in brain, pancreatic and breast cancer cells. When the research team removed all NIK expression using CRISPR-Cas9 genome editing, the cancer cells were no longer able to invade. On the other hand, NIK is upregulated when a cell becomes cancerous, and the more invasive tumors had higher activation of the NIK pathway.
In cancer cells, mitochondria typically undergo fission and are small in size, allowing them to move rapidly to areas of the cell with high energy demands—usually the branches of a cell that are invading surrounding tissue. Without NIK, the mitochondria become fused and are impaired in their ability to move efficiently to areas of the cell that initiate and drive the process of invasion.
Under normal circumstances, when mitochondria have plenty of NIK, they can morph into different shapes, from something like a slow, hulking bus to a nimble race car. “Mitochondria are very dynamic and can split, fuse and move in the cell,” said Raquel Sitcheran, PhD, assistant professor at the Texas College of Medicine and corresponding author of the paper. “When they’re smaller, they can get where they need to go much more easily. There’s a link between NIK, mitochondrial function and cancer cell invasion. It gives us a new angle in thinking about the role of mitochondria in cancer progression.”
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