An Epigenetic Change Causes the Block of Antitumor Genes
News Jun 12, 2013
This balance is disrupted in tumor cells. There are many causes, for example, the existence of mutations, but also the acquisition of a chemical signal, methylation, which blocks the activity of genes that stop cancer growing. It is unknown, however, what happens in the cells after they have acquired this epigenetic alteration.
Researchers of the IDIBELL, led by Manel Esteller, director of the Epigenetics and Cancer Biology Program, ICREA researcher and professor at the University of Barcelona, describe in the online edition of the journal Oncogene how this methylation triggers a dimensional change in the nucleus cell to form spherical structures called nucleosomes that block the function of antitumor genes.
Researchers observed that genes that protect from cancer as the vitamin A receptor alter its activity in colon cancer cells by the presence of spherical structures formed by DNA (in this case expression regulatory regions of genes) and proteins called histones.
"We have observed," said the researcher Manel Esteller, "that epigenetic drugs, capable of demethylating DNA, approved for patients with a subtype of leukemia, are also able to eliminate these 'balls' of antitumor genes so that they can express again, and recover their function."
“This study”, explained Esteller, “also served to discover new genes, inhibitors of cancer.”
The discovery increases the molecular understanding of the causes of cancer and as to the clinical application of the discovery; Esteller explained that "there is currently a wide range of drugs in preclinical development capable of ejecting nucleosomes of aberrant places of the genome".
Tight junctions are multi-protein complexes that serve as barriers in epithelial tissues such as the skin or lining of the gut. Loss of a specific tight junction barrier protein, claudin 18, occurs in the majority of gastric cancer patients and is correlated with poor prognosis in patients with advanced gastric cancer.READ MORE