CHAMPAIGN, Ill. Researchers have discovered a mechanism by which Helicobacter pylori, the only known cancer-causing bacterium, disables a tumor suppressor protein in host cells.
The new study, in the journal Oncogene, reports the discovery of a previously unknown mechanism linking H. pylori infection and stomach cancer, the second leading cause of cancer deaths worldwide.
About two-thirds of the world's population is infected with H. pylori, a bacterium that can survive in the harsh environment of the stomach. Most infected people never develop disease. For a significant minority, however, infection with H. pylori leads to inflammation, ulcers and in some cases, stomach (gastric) cancer.
H. pylori's ability to cause disease is closely associated with a virulence protein called CagA. Previous studies have found that CagA-positive strains are much more likely to cause inflammation and spur the abnormal cell division and growth of cells that lead to cancer.
H. pylori injects CagA into the epithelial cells that line the stomach. Within the cells, CagA is able to hijack various signaling pathways and disrupt proper cellular functions.
Other studies have identified RUNX3 (pronounced RUNKS-three) as an important gastric cancer tumor suppressor.
Loss of expression of RUNX3 is causally associated with the development of gastric cancer, said University of Illinois medical biochemistry professor Lin-Feng Chen, who led the study. RUNX3 guards against tumor formation by spurring the production of factors that target unhealthy cells for destruction.
"Although emerging evidence suggests that RUNX3 is a tumor suppressor whose inactivation is involved in the initiation and progression of gastric cancer," the authors wrote, "the trigger for RUNX3 inactivation within gastric cells is largely unknown."
"The protein, RUNX3, is a transcription factor, so it activa
|Contact: Diana Yates, Life Sciences Editor|
University of Illinois at Urbana-Champaign