Scientists at Johns Hopkins have identified a tiny bit of genetic code, which helps the p53 gene to kill the colon cancer cells.
The genetic code is called miR-34a, a microRNA which participates in p53's uncanny ability to kill cells that are likely to become malignant because of damaged genes in their nuclei.
MicroRNAs are small chains of ribonucleic acid (RNA), which stick to messenger RNAs, and prevent proteins from being made.
Dr. Josh Mendell, Assiatant Professor in the McKusick-Nathans Institute of Genetic Medicine, suspected that p53 activates microRNAs like miR-34a, for various studies have demonstrated that these tiny RNA molecules are frequently abnormal in cancer cells.
"P53 is one of the most commonly mutated genes in human cancers. And there is now a great deal of evidence that microRNAs themselves can act to either promote cancer or to stop cancer spread," says Mendell.
During the study, the researchers chemically damaged the DNA of two sets of colon cancer cells, one missing p53 and the other containing healthy p53. Thereafter, they looked for any of the 500 known human microRNAs that were activated only in cells containing p53.
They found that the miR-34a gene was turned on by p53, and that p53 bound directly to the genetic material near miR-34a to promote its activation. This indicates that p53 controls miR-34a.
When the researchers put miR-34a into colon cancer cells in further experiments, the found that it killed cells that contained p53, but fewer were killed in cells lacking p53. This indicates that microRNA gets its kill orders from p53.
Upon examination of pancreatic cancer cells known to contain damaged or missing p53, the researchers found that the cells had limited or zero miR-34a.
"With no p53 gene or miR-34a to stem tumor development, there's no brake in pancreatic cells and uncontrolled growth leads to cancer," says Dr. Anirban Maitra, Associate Professor of Pathology, Oncology and Genetic Medicine.
The researchers are now looking for missing miR-34a in other cancers. If this turns out to be a widespread phenomenon, the work may lead to treatments that aim to restore the missing microRNA to cancer cells.