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Novel 'on-off switch' mechanism stops cancer in its tracks
September 24, 2009A tiny bit of genetic material with no previously known function may hold the key to stopping the spread of cancer, researchers at Yale School of Medicine and Sichuan University in Chengdu, China report in two papers in the September 7-11 issue of Proceedings of the National Academy of Sciences.
In the papers, Alan Garen of the Department of Molecular Biophysics & Biochemistry at Yale and his colleague Xu Song explain how cancer may overcome an organism's natural "stop sign" for cell division.
During early development, stem cells give rise to other cells that differentiate into all types of tissue. New cell division and proliferation stop as the organism matures. However, cancer can hijack this process and trigger the uncontrolled cell division that produces cancer tumors.
One mechanism that stops cell proliferation is a family of tumor-suppressor proteins (TSP) that bind to and block the function of proto-oncogenes, or genes that have the potential to trigger cancer.
Garen's team working with mice found that an RNA molecule from an area of the genome that does not produce proteins prevents a type of TSP from inactivating these incipient cancer genes. The TSP protein they studied, called PSF, is virtually identical in mice and humans, he said.
The Yale team succeeded in preventing the formation of tumors in mice by either increasing the amount of PSF or decreasing the amount of the non-coding RNA in a cell.
"The tumor cell stops proliferating and the tumor regresses in a mouse model of cancer, suggesting that both procedures could be the basis of a clinical protocol," said Garen, who is a member of Yale Cancer Center.
Garen and his colleagues plan to continue their studies on the mechanism that regulates the amount of PSF-binding RNA in a cell, which they believe is central to the origins of cancer.
Yale University
One mechanism that stops cell proliferation is a family of tumor-suppressor proteins (TSP) that bind to and block the function of proto-oncogenes, or genes that have the potential to trigger cancer.
Garen's team working with mice found that an RNA molecule from an area of the genome that does not produce proteins prevents a type of TSP from inactivating these incipient cancer genes. The TSP protein they studied, called PSF, is virtually identical in mice and humans, he said.
The Yale team succeeded in preventing the formation of tumors in mice by either increasing the amount of PSF or decreasing the amount of the non-coding RNA in a cell.
"The tumor cell stops proliferating and the tumor regresses in a mouse model of cancer, suggesting that both procedures could be the basis of a clinical protocol," said Garen, who is a member of Yale Cancer Center.
Garen and his colleagues plan to continue their studies on the mechanism that regulates the amount of PSF-binding RNA in a cell, which they believe is central to the origins of cancer.
Yale University
Cell Division Current Events and Cell Division News RSSParadoxical protein might prevent cancer
One difficulty with fighting cancer cells is that they are similar in many respects to the body's stem cells. By focusing on the differences, researchers at Karolinska Institutet have found a new way of tackling colon cancer. The study is presented in the prestigious journal Cell.
Study reveals why certain drug combinations backfire
Combination drug therapy has become a staple for treating many infections. For instance, doctors treat extensively drug resistant forms of tuberculosis with one drug that breaks down the pathogen's protective barriers and opens the door for another to deliver the deathblow.
Sponges recycle carbon to give life to coral reefs
Coral reefs support some of the most diverse ecosystems on the planet, yet they thrive in a marine desert. So how do reefs sustain their thriving populations?
Researchers discover mechanism that prevents two species from reproducing
Cornell researchers have discovered a genetic mechanism in fruit flies that prevents two closely related species from reproducing, a finding that offers clues to how species evolve.
Common weed could provide clues on aging and cancer
A common weed and human cancer cells could provide some very uncommon details about DNA structure and its relationship with telomeres and how they affect cellular aging and cancer, according to a team led by scientists from Texas A&M University and the University of Cincinnati (UC).
Boston University scientists first to see RNA network in live bacterial cells
Scientists who study RNA have faced a formidable roadblock: trying to examine RNA's movements in a living cell when they can't see the RNA. Now, a new technology has given scientists the first look ever at RNA in a live bacteria cell-a sight that could offer new information about how the molecule moves and works.
Texas A&M researchers find new mechanism for circadian rhythm
Molecules that may hold the key to new ways to fight cancer and other diseases have been found to play an important role in regulating circadian rhythm, says Liheng Shi, a researcher in Texas A&M's Department of Veterinary Integrative Biosciences.
Checkered history of mother and daughter cells explains cell cycle differences
When mother and daughter cells are created each time a cell divides, they are not exactly alike. They have the same set of genes, but differ in the way they regulate them.
Eutrophication affects diversity of algae
Eutrophication of the seas may have an impact on genetic variation in algae, research at the University of Gothenburg shows.
MDC scientists show how hematopoietic stem cell development is regulated
During cell division, whether hematopoietic stem cells (HSCs) will develop into new stem cells (self-renewal) or differentiate into other blood cells depends on a chemical process called DNA methylation.
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