This protein helps cancer cells survive treatment—and points to new treatments
Why it matters: Understanding Bcl-2's mechanism could lead to new cancer therapies by targeting its protective function against cell death.
- Umeå University researchers discovered that the protein Bcl-2 protects cancer cells by capturing and binding multiple death-inducing Bax proteins, making cell death inhibition more efficient than previously understood.
- Bcl-2 is often overproduced in nearly half of all human cancers, promoting tumor growth and leading to poor treatment response by preventing Bax from initiating apoptosis.
- Advanced neutron experiments were used to demonstrate how Bcl-2, located on the outer mitochondrial surface, can simultaneously bind several Bax proteins, enhancing its protective function against cell death.
- Cardiolipin, a specific lipid in the mitochondrial membrane, can promote apoptosis, but even its presence is insufficient to overcome the protective effect of sufficiently high Bcl-2 levels.
- Gerhard Gröbner, lead author, suggests this knowledge could pave the way for new cancer treatments by specifically targeting Bcl-2 and its protective function.
Researchers at Umeå University have uncovered a crucial mechanism by which cancer cells evade programmed cell death, or apoptosis, a process often triggered by treatments like chemotherapy. Their study reveals that the protein Bcl-2 efficiently blocks the cell-killing protein Bax, even at moderate levels, by binding multiple Bax proteins simultaneously on the mitochondrial surface, making cancer cells resistant to therapy.
