STARD7: a key link between metabolism, mitochondria and breast cancer
To support enhanced proliferation, cancer cells must reprogram their metabolism. They adjust how they use energy resources, drawing heavily on key cellular organelles like mitochondria—often referred to as the cell’s “powerhouses.” However, mitochondria require a supply of lipids from another organelle, the endoplasmic reticulum, to properly function. This transfer is handled by specialized proteins, including STARD7, whose role in breast cancer cells has just been brought to light.
The team led by Alain Chariot (Laboratory of Medical Chemistry, WELRI Investigator) found that when STARD7 is missing, cells undergo a metabolic shift. One specific metabolite, SAM (S-Adenosyl-L-methionine) accumulates in cells. This molecule, known for its role in epigenetic regulation, leads to an excessive methylation of some histones, the proteins that package DNA. As a result, the expression of many genes involved in cell cycle progression is repressed, slowing down cell division.
But that’s not all. The absence of STARD7 also disrupts key signaling pathways involved in breast cancer. Signaling via ERα receptors (linked to hormone-dependent cancers) and EGFR receptors (whose activity is often enhanced in triple-negative breast cancers) is impaired. In cells lacking STARD7, EGFR receptors are not properly recycled to the cytoplasmic membrane, which impairs their overall function.
In short, this study highlights STARD7’s central role at the crossroads of metabolism, mitochondrial function and cancer cell proliferation. A discovery that could pave the way for new research avenues to better understand, and perhaps one day, better treat breast cancer.
