Precision Medicine has a New Target
Researchers at the Centre for Cancer Biomedicine, a Center of Excellence and a member of Oslo Cancer Cluster, have discovered an enzyme wreaking havoc inside cells that turns into tumors.
For our body to work as normal, cells need to know which way is up. When cells lose track of their orientation, they can start to grow out of control, and develop into cancer.
A team of researchers has identified an enzyme for cell orientation, offering a future target for precision medicine in cancer treatment.
– We have discovered how a traffic jam in the sorting inside cells can cause tumor development, says senior author Tor Erik Rusten at the Centre for Cancer Biomedicine at the University of Oslo and Oslo University Hospital.
LKB1 Activity Promotes Tumor Growth
And the villain is an enzyme called LKB1. Results suggests that LKB1 is shut off in normal cells, but that a traffic jam allows LKB1 to remain active longer.
– High activity of LKB1 contributes to tumor growth by sending confusing signals to the cell about which way is up, says Rusten.
The teams research showed that a high activity of LKB1 increased stress signals in the cells and disrupted cellular orientation.
Targeting LKB1 as Potential Therapy
Rusten and colleagues further tested the effect of genetically removing LKB1 from cells that otherwise would form tumors due to loss of orientation.
– To our surprise, reducing LKB1 activity restored normal epithelial organization and prevented tumor growth. These results suggest that pharmacological inhibition of LKB1 may be beneficial as treatment in some cancer types, says Rusten.
It will be important to determine if pharmacological agents can specifically target LKB1 in animals or in human cells in culture, and how such potential treatment may be transferred to the clinic.
– This is another example on how long-term financial commitments to basic research can lead to high-quality preclinical results. Hopefully, our findings will help provide better treatment for future cancer patients, concludes Rusten
