How cancer-promoting gene accelerates the diseaseJanuary 24th, 2009 - 2:09 pm ICT by ANI
London, January 24 (ANI): Scientists at the University of California San Francisco (UCSF) say that they have found out a new mechanism whereby a much-studied cancer-promoting gene accelerates the disease.
Dr. Davide Ruggero and Dr. Maria Barna, who led the study, say that their finding suggests a new strategy to halt cancers progress.
Most studies to date have largely focused on how the mutated gene, Myc, disrupts the ability of DNA to be transcribed into RNA the first step in making proteins that are essential for cell growth and function.
However, the current study has for the first time shown that the altered Myc gene, called an oncogene, can also act directly on the final stage of protein production.
The researchers say that the finding in mice suggests that drugs already available to counter increased protein production could slow or stop cancers runaway growth induced by Myc.
Control of protein production rapidly affects cell behavior, and in a robust manner, Nature magazine quoted Ruggero, assistant professor of urology at the UCSF Helen Diller Family Comprehensive Cancer Center and co-senior author on the paper with Barna, as saying.
The ability of the Myc oncogene to directly alter this process may well explain the rapid progression of cancer formation, the researcher added.
The researchers said that though it had been known for some time that Myc gene becomes an oncogene as a result of mutation and interferes with the early steps in DNA activity in the cell nucleus, but it affected the subsequent production of proteins, a step known as translation, was unknown.
A cancer causing gene, such as Myc, regulates many distinct cellular processes, and that can make it very difficult to tease apart which ones are the most important for the cancer to progress, says Barna, a faculty fellow in the UCSF biochemistry and biophysics department.
The key to our studies was the ability to generate novel genetic tools to halt Mycs action on protein production. This demonstrates how essential this process is for cancer formation, Barna adds.
With an eye on determining whether protein production induced by Myc played a role in cancer, the researchers genetically crossed two types of mice one that was cancer-prone and overexpressed the Myc oncogene, and the other that was newly engineered to lower protein production.
According to the researchers, the new cross of mice possessed not only the well-known destructive Myc traits, but also an enhanced ability to damp down protein production.
In these mice, the restrained protein production restored to near-normal the cell growth, division and protective cell-sacrifice needed to counter cancer.
The research team also observe that the increased control over the so-called translation of RNA into proteins countered damage to chromosome function otherwise caused by Myc, and preserved functions vital to faithful cell division.
They point out that changes in the genetic integrity of cells are recognized as hallmarks of cancer, and the new findings show that Myc can cause these abnormalities through control of protein production.
The scientists say that the research suggests that Myc may disrupt a number of genes downstream of its damage to DNA.
We discovered a previously unrecognized link between alterations in protein synthesis and the mechanism by which cells maintain the integrity of the genome. We found
that when Myc is overexpressed, this leads to changes in protein levels of a key gene that is essential for normal distribution of genetic material between daughter cells during cell division, Ruggero stresses
Based on the findings, he came to the conclusion that halting Mycs action on protein production with targeted therapies could prevent harmful genetic changes in cells that lead to cancer progression. (ANI)
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