Leukaemia Cells are Addicted to Vitamin B6
Researchers from the Cold Spring Harbor Laboratory (CSHL) and Memorial Sloan Kettering Cancer Center (MSK) have discovered that Acute Myeloid Leukaemia (AML) grows by taking advantage of the B6 vitamin to accelerate cell division. Published in Cell, the findings could pave the way for a treatment that can stop cancer growth by manipulating the enzyme that pushes B6 to make proteins essential for cell division. Normal healthy cells need vitamin B6 to survive, so targeting the enzyme will allow healthy cells to live whilst attacking cancerous cells.
AML is an aggressive form of blood cancer where an excess of immature white blood cells or a myeloid line of blood-forming cells are made by the bone marrow. It’s very rare, and only one-third of AML patients will survive five years after diagnosis. The researchers investigated how AML achieves rapid growth and turned to the genomes of these cancerous cells to find out.
More than 230 genes were found to be very active in leukemic cells, and using CRISPR/Cas9, the activity of each of these genes was halted to find out what would happen to the cancer cells. One particular finding was in the gene that produces PDXX, an enzyme that facilitates the usage of vitamin B6 in cells which proved to be the most important for cancer growth.
Different studies have found links between vitamins and cancer growth, but the findings of vitamin B6 in this study is a new and unexpected one.
Vitamin B6 is essential for some enzymes to work correctly for cell growth. The PDXK enzyme pushes the activity of B6 during cell division, and because normal healthy cells don’t divide all the time, it’s not always active. Cancer cells divide more frequently than normal cells. The researchers saw that the PDXK enzyme was constantly pushing B6 activity and they showed that leukemic cells are essentially addicted to vitamin B6.
This new information could be useful for developing a new drug that could specifically block the proliferation of leukemic cells by blocking enzyme PDXK. AML patients won’t benefit from a reduced dietary intake of vitamin B6 as healthy cells need this vitamin to function. A drug targeting the PDXK enzyme could possibly slow or stop the growth of cancerous cells, without the side effects that eliminating B6 completely would have on healthy cells.