In the process of cell division genome will be copied into two copies. This process occurs in called replication fork structure. In tumor cells, the replication forks are often destroyed, causing double-stranded DNA rupture.
By the university of Geneva, Switzerland, a professor at the school science Thanos Halazonetis leadership of an international study, reveals how cancer cells to repair damaged replication forks to complete the cell division. This is called "rupture induced copy" (BIR) signaling pathways in cancer cells in common, but it is rare in healthy cells. Published in the journal Science (Science) of the study, which reveals a significant difference between two types of cells, the authors will try to use it to achieve therapeutic purposes.
Our cells to generate two daughter cells proliferation, must first to replicate by 6.4 billion nucleotides of DNA. Like a zipper to open the double-stranded DNA, generating "replication forks", a group of enzymes move along the replication forks to complete DNA replication. In different areas of the DNA replication forks will change its position as the copy process.
Cell proliferation was called as proto-oncogene special control of some specific genes. Proto-oncogene expression or mutation will trigger a runaway sexual proliferation, promote cancer growth. "In tumor cells, the proto-oncogenes induced the replication fork collapse or destruction. This can lead to replication complex separation of enzyme, double chain rupture, "professor at the university of Geneva molecular biology Thanos Halazonetis said.
Exist in the same mechanism in the yeast and malignant cells
With the Finnish Helsinki university, university of duisburg, Germany - eisen, the United States at brandeis university and the Swedish Karolinska institutet, a geneticist at the team identified the repair the damaged mechanism of replication fork so that the copy was restored. The researchers analyzed 690 genes related to metabolism of DNA. "We set up a siRNAs library, siRNAs is a kind of can prevent them from expression of these molecules targeted genes, one at a time," lead author of the paper, the research team postdoctoral researcher Lorenzo Costantino says the report.
Use of these genetic hook, the researchers isolated several genes needed for replication forks to repair damaged, including POLD3 and POLD4. The two genes encoding proteins related to DNA replication and repair. "Thanks to these first hit, we identified a called 'fracture induced by copying (BIR) of different repair process, this process is known to exist in the yeast, rather than human normal cells," study co-author, Dr Team researchers Sotirios Sotiriou said.
Abnormal tumor DNA replication
Biologists have found that very few BIR repair process for use by healthy cells, are very common in human tumor cells. In addition, the use of this one repair intracellular signaling pathways can explain, cancer cells observed anomalies of some parts of the genome replication is how to happen. In fact, genome instability is necessary for tumor formation, as it allows the necessary mutation accumulation. "Such as POLD3 and POLD4 different protein is to recruit BIR repair process. Our next goal is to identify all the intracellular signaling pathways related other biochemical effect factor, thus determine which could become targets of therapy, "Thanos Halazonetis said.
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