BYU microbiologist Kim O’Neill (seated), shown here with doctoral student Fan Zhang (standing), has worked to test the effect of caffeine on cancer cells. Preliminary tests indicate that caffeine may keep cancer cells alive when they should die.
By Julie Walker
While caffeine’s role as a carcinogen has been widely debated, a new study suggests that caffeine may act as an advocate to cancer cells, extending their lives and allowing them to spread.
A BYU researcher found that while it doesn’t fit the classic model of a carcinogen–a substance that damages healthy cells–in some circumstances, caffeine may protect cancer cells from death.
“Cancer is a disease where cell division has gone out of control. In some cases, the cell does not know how to die. We have found that caffeine may inhibit the apoptotic mechanism–the cell’s own defensive mechanism–and keep damaged cells alive when they should die,” says microbiologist Kim O’Neill of BYU’s Cancer Research Center.
O’Neill published the report in the December 1997 issue of Cancer Letters, an international scientific journal.
O’Neill says the study is interesting basic science but that it does not provide enough information to determine whether consuming caffeine poses any health risk.
“This is just a small piece of work that indicates that, under certain conditions, caffeine may suppress apoptosis or the induction of apoptosis in vitro, but the relevance of that may not be known for several years,” he says.
One of the body’s main defense mechanisms, the process of apoptosis or “cell suicide” helps eliminate damaged cells before they threaten the body. Virtually every cell in the body is preprogrammed to undergo apoptosis when DNA is damaged, or when the cell is no longer needed.
Some cells, such as skin cells, die and are replaced frequently while others, such as nerve cells, are with the body from birth to death. Generally, when DNA from a cell is damaged, by chemicals or other means, the cell’s own internal apoptotic mechanism switches on.
“Apoptosis is the efficient way for a cell to die because it will pass on some of its good contents to neighboring cells and eliminate damaged cells that could pass on defective DNA. The apoptotic mechanism allows the cells to protect their DNA, keep it intact and pure, so damaged DNA won’t be passed on to the next generation,” says O’Neill.
Many new cancer thera-pies aim to activate the cell’s own preprogrammed “suicide” mechanism to eliminate cancer cells. By intentionally creating breaks in the DNA, the therapies send a message to the damaged cells to initiate apoptosis.
O’Neill says that if the cell is not allowed to undergo apoptosis, then cancerous cells may be allowed to spread, and precancerous cells may be allowed to progress.
“If you had, for example, a damaged precancerous cell and the cell is saying ‘I’ve gotta die, I’ve gotta die,’ and you stop the method by which it can die, then there’s a chance that the cell will become cancerous,” says O’Neill.
For the caffeine tests, O’Neill dosed leukemia cells with caffeine and then followed a common heat shock procedure designed to induce cell death. Under normal conditions, the test would show breaks in the DNA, followed by a sequence of events that lead to cell death. But when the cancer cells were boosted with caffeine before receiving the deadly heat shock, they refused to die.
“Normally, by exposing cells to heat shock for about an hour, 12 hours later those cells will undergo apoptotic death. By adding caffeine to the medium, you prevent the death of the cancer cells and therefore give them protection against this programmed cell death. Since they appear unaffected by the heat shock, the cancerous cells can continue to replicate,” he says.
The caffeine studies were conducted using the “comet assay,” a new test that allows researchers to see the effects of chemicals on human cells, and to quantify damage to DNA. O’Neill, one of the pioneers in the development of the comet assay, previously used the test to determine that caffeine may also inhibit a cell’s ability to repair its damaged DNA.
