This is the first evidence that cyclin B1/Cdk1both senses the cell's energy needs during the G2/M transition and communicates that information to mitochondria. This mechanism could be an appealing therapeutic target for cancer.
"Under stress from radiation or chemotherapy, tumor cells may need mitochondria to provide extra energy to repair DNA damage," said Li. "If we block this communication between nucleus and mitochondria in tumor cells and inhibit glycolysis (directly converting glucose into cellular energy, the major cellular fuel for cancer cells), this could be a new approach to treating cancer."
In addition to making radiation and chemotherapy more effective, modulating cellular energy could potentially be used to control tumor growth.
"Like cars, tumors need a lot of gas," said Li. "If we reduce the amount of gas, we could perhaps slow down the cancer."
While inhibiting mitochondrial energy production could control tumors, boosting this process could help regenerative cells in normal tissues, such as muscle stem cells, repair damaged tissue, opening an entirely different therapeutic window.
Ironically, this newly discovered cellular mechanism could also boost communication between scientists, as this research unites two disciplines that had previously been separate: cell cycle and mitochondrial studies.
"A lot of people are working in mitochondria, and many more study the cell cycle, but few are studying the relationship between them," said Li. "In this paper, we show cross-talk between the nucleus and mitochondria. Now, perhaps, we can get similar cross-talk among experts between these two areas of study."
|Contact: Dorsey Griffith|
University of California - Davis Health System