New Study Proves That Abnormal Cell Division Will Promote The Occurrence of Tumor Cell

In a recent study published in the Journal of Nature, researchers at the University of Geneva found that premature entry of the genome into the replication phase can trigger molecular collisions and new mutations in DNA molecules. Relevant findings are expected to help researchers develop new therapies to treat cancer.

The accumulation of mutations in the human genome usually is the source of cancer and cancer resistance to therapy. In the process of cell division, Cyclin E and Myc genes are often active. While the response to carcinogens mutating, these genes induce cells to prematurely replicate DNA during the cell cycle. The abnormal cell division will promote the occurrence of tumor, then what makes this happen?

When a cell divides into two progeny cells, it must replicate the entire genome and partially transcribe it into protein molecules. Cell division is regulated by specific genes, including the oncogenes Cyclin E and Myc, whose overexpression or Mutations that become oncogenes, which are subsequently exposed to carcinogens, induce uncontrolled cell proliferation and promote cancer. Researchers want to figure out why there are a number of mutations that accumulate in cancer-activated cells in this study.

Replication must occur between two genesIn order to replicate the entire DNA, that is, replicate nearly 6.4 billion pairs of nucleotide base pairs in a matter of hours, cells need to be prepared simultaneously at thousands of sites per chromosome, and replication origins need to be well controlled to ensure that replication can be done in a smooth and efficient manner.

Researchers have developed a new method to identify the origin of replication for all chromosomes, including the isolation and sequencing of newly synthesized DNA molecules in cells that enter the replication phase in order to map the genomic sites at the start of replication Methods developed for human cells may provide higher sensitivity and resolution. Morgane Macheret, one of the researchers said that, ‘cells were able to identify all possible origins of replication by molecular markers initially and we found that abnormal origins of replication may then be eliminated in normal cells, which is the situation inside genes, where the origin of replication is located outside the gene so that the complete information for each gene can be retained.’

On the other hand, the activation of the oncogenes Cyclin E and Myc can induce cells to prematurely replicate DNA while not eliminating all the origin of replication that is present in the gene. The replication and transcription machinery is also active in the genes that carry the origin of replication, creating some conflicts. Researchers have shown that these "clashes" will induce DNA fragmentation, chromosomal rearrangements and mutations.

In order to confirm whether the above findings can explain the genomic instability that exists in different types of cancer, researchers have studied more than 500,000 chromosomal rearrangements exhibited by many tumors and found that chromosomal abnormalities were particularly pronounced in the areas of conflict described by the researchers. Therefore, the researchers believe that the results of this study can explain the genetic origin of genomic instability in tumors, or provide some ideas and thoughts for the development of new anti-cancer therapy in the near future.

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